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Publications of Staci D. Bilbo    :chronological  alphabetical  combined listing:

%% Journal Articles   
@article{fds342148,
   Author = {Kopec, AM and Smith, CJ and Bilbo, SD},
   Title = {Neuro-Immune Mechanisms Regulating Social Behavior: Dopamine
             as Mediator?},
   Journal = {Trends in Neurosciences},
   Volume = {42},
   Number = {5},
   Pages = {337-348},
   Year = {2019},
   Month = {May},
   url = {http://dx.doi.org/10.1016/j.tins.2019.02.005},
   Abstract = {Social interactions are fundamental to survival and overall
             health. The mechanisms underlying social behavior are
             complex, but we now know that immune signaling plays a
             fundamental role in the regulation of social interactions.
             Prolonged or exaggerated alterations in social behavior
             often accompany altered immune signaling and function in
             pathological states. Thus, unraveling the link between
             social behavior and immune signaling is a fundamental
             challenge, not only to advance our understanding of human
             health and development, but for the design of comprehensive
             therapeutic approaches for neural disorders. In this review,
             we synthesize literature demonstrating the bidirectional
             relationship between social behavior and immune signaling
             and highlight recent work linking social behavior, immune
             function, and dopaminergic signaling in adolescent neural
             and behavioral development.},
   Doi = {10.1016/j.tins.2019.02.005},
   Key = {fds342148}
}

@article{fds342605,
   Author = {Smith, CJ and Bhanot, A and Norman, E and Mullett, JE and Bilbo, SD and McDougle, CJ and Zürcher, NR and Hooker, JM},
   Title = {A Protocol for Sedation Free MRI and PET Imaging in Adults
             with Autism Spectrum Disorder.},
   Journal = {Journal of Autism and Developmental Disorders},
   Year = {2019},
   Month = {April},
   url = {http://dx.doi.org/10.1007/s10803-019-04010-3},
   Abstract = {Imaging technologies such as positron emission tomography
             (PET) and magnetic resonance imaging (MRI) present
             unparalleled opportunities to investigate the neural basis
             of autism spectrum disorder (ASD). However, challenges such
             as deficits in social interaction, anxiety around new
             experiences, impaired language abilities, and
             hypersensitivity to sensory stimuli make participating in
             neuroimaging studies challenging for individuals with ASD.
             In this commentary, we describe the existent training
             protocols for preparing individuals with ASD for PET/MRI
             scans and our own experience developing a training protocol
             to facilitate the inclusion of low-functioning adults with
             ASD in PET-MRI studies. We hope to raise awareness of the
             need for more information exchange between research groups
             about lessons learned in this context in order to include
             the entire disease spectrum in neuroimaging
             studies.},
   Doi = {10.1007/s10803-019-04010-3},
   Key = {fds342605}
}

@article{fds342359,
   Author = {Smith, CJ and Bilbo, SD},
   Title = {Microglia Sculpt Sex Differences in Social
             Behavior.},
   Journal = {Neuron},
   Volume = {102},
   Number = {2},
   Pages = {275-277},
   Year = {2019},
   Month = {April},
   url = {http://dx.doi.org/10.1016/j.neuron.2019.03.039},
   Abstract = {Microglia are increasingly recognized as developmental
             sculptors of neural circuits. In this issue of Neuron,
             VanRyzin et al. (2019) demonstrate a novel mechanism by
             which endocannabinoids drive microglia to phagocytose
             newborn astrocytes in the medial amygdala of male rats,
             promoting sex differences in social play
             behavior.},
   Doi = {10.1016/j.neuron.2019.03.039},
   Key = {fds342359}
}

@article{fds341885,
   Author = {Liu, X and Nemeth, DP and McKim, DB and Zhu, L and DiSabato, DJ and Berdysz, O and Gorantla, G and Oliver, B and Witcher, KG and Wang, Y and Negray, CE and Vegesna, RS and Sheridan, JF and Godbout, JP and Robson,
             MJ and Blakely, RD and Popovich, PG and Bilbo, SD and Quan,
             N},
   Title = {Cell-Type-Specific Interleukin 1 Receptor 1 Signaling in the
             Brain Regulates Distinct Neuroimmune Activities.},
   Journal = {Immunity},
   Volume = {50},
   Number = {3},
   Pages = {764-766},
   Year = {2019},
   Month = {March},
   url = {http://dx.doi.org/10.1016/j.immuni.2019.02.012},
   Abstract = {© 2019 (Immunity 50, 317-333.e1–e6; February 19, 2019)
             Main Text: In the original version of the published
             manuscript, the insets of Figure 3F (middle and right
             panels) were identical to the insets of Figure 3E. This
             error was generated inadvertently during the revision
             process of the manuscript. The insets of Figure 3F (middle
             and right panels) have now been replaced and are consistent
             with their corresponding images, and the revised version is
             provided below and has been corrected online. The authors
             apologize for the error. [Figure presented]},
   Doi = {10.1016/j.immuni.2019.02.012},
   Key = {fds341885}
}

@article{fds341510,
   Author = {Liu, X and Nemeth, DP and McKim, DB and Zhu, L and DiSabato, DJ and Berdysz, O and Gorantla, G and Oliver, B and Witcher, KG and Wang, Y and Negray, CE and Vegesna, RS and Sheridan, JF and Godbout, JP and Robson,
             MJ and Blakely, RD and Popovich, PG and Bilbo, SD and Quan,
             N},
   Title = {Cell-Type-Specific Interleukin 1 Receptor 1 Signaling in the
             Brain Regulates Distinct Neuroimmune Activities.},
   Journal = {Immunity},
   Volume = {50},
   Number = {2},
   Pages = {317-333.e6},
   Year = {2019},
   Month = {February},
   url = {http://dx.doi.org/10.1016/j.immuni.2018.12.012},
   Abstract = {Interleukin-1 (IL-1) signaling is important for multiple
             potentially pathogenic processes in the central nervous
             system (CNS), but the cell-type-specific roles of IL-1
             signaling are unclear. We used a genetic knockin reporter
             system in mice to track and reciprocally delete or express
             IL-1 receptor 1 (IL-1R1) in specific cell types, including
             endothelial cells, ventricular cells, peripheral myeloid
             cells, microglia, astrocytes, and neurons. We found that
             endothelial IL-1R1 was necessary and sufficient for
             mediating sickness behavior and drove leukocyte recruitment
             to the CNS and impaired neurogenesis, whereas ventricular
             IL-1R1 was critical for monocyte recruitment to the CNS.
             Although microglia did not express IL-1R1, IL-1 stimulation
             of endothelial cells led to the induction of IL-1 in
             microglia. Together, these findings describe the structure
             and functions of the brain's IL-1R1-expressing system and
             lay a foundation for the dissection and identification of
             IL-1R1 signaling pathways in the pathogenesis of CNS
             diseases.},
   Doi = {10.1016/j.immuni.2018.12.012},
   Key = {fds341510}
}

@article{fds339917,
   Author = {Rivera, PD and Hanamsagar, R and Kan, MJ and Tran, PK and Stewart, D and Jo, YC and Gunn, M and Bilbo, SD},
   Title = {Removal of microglial-specific MyD88 signaling alters
             dentate gyrus doublecortin and enhances opioid
             addiction-like behaviors.},
   Journal = {Brain Behav Immun},
   Volume = {76},
   Pages = {104-115},
   Year = {2019},
   Month = {February},
   url = {http://dx.doi.org/10.1016/j.bbi.2018.11.010},
   Abstract = {Drugs of abuse promote a potent immune response in central
             nervous system (CNS) via the activation of microglia and
             astrocytes. However, the molecular mechanisms underlying
             microglial activation during addiction are not well known.
             We developed and functionally characterized a novel
             transgenic mouse (Cx3cr1-CreBTtg/0:MyD88f/f [Cretg/0])
             wherein the immune signaling adaptor gene, MyD88, was
             specifically deleted in microglia. To test the downstream
             effects of loss of microglia-specific MyD88 signaling in
             morphine addiction, Cretg/0 and Cre0/0 mice were tested for
             reward learning, extinction, and reinstatement using a
             conditioned place preference (CPP) paradigm. There were no
             differences in drug acquisition, but Cretg/0 mice had
             prolonged extinction and enhanced reinstatement compared to
             Cre0/0 controls. Furthermore, morphine-treated Cretg/0 mice
             showed increased doublecortin (DCX) signal relative to
             Cre0/0 control mice in the hippocampus, indicative of
             increased number of immature neurons. Additionally, there
             was an increase in colocalization of microglial lysosomal
             marker CD68 with DCX+cells in morphine-treated Cretg/0 mice
             but not in Cre0/0 or drug-naїve mice, suggesting a specific
             role for microglial MyD88 signaling in neuronal phagocytosis
             in the hippocampus. Our results show that MyD88 deletion in
             microglia may negatively impact maturing neurons within the
             adult hippocampus and thus reward memories, suggesting a
             novel protective role for microglia in opioid
             addiction.},
   Doi = {10.1016/j.bbi.2018.11.010},
   Key = {fds339917}
}

@article{fds340827,
   Author = {Missig, G and Robbins, JO and Mokler, EL and McCullough, KM and Bilbo,
             SD and McDougle, CJ and Carlezon, WA},
   Title = {Sex-dependent neurobiological features of prenatal immune
             activation via TLR7.},
   Journal = {Molecular Psychiatry},
   Year = {2019},
   Month = {January},
   url = {http://dx.doi.org/10.1038/s41380-018-0346-4},
   Abstract = {Immune activation during pregnancy via infection or
             autoimmune disease is a risk factor for neuropsychiatric
             illness. Mouse models of prenatal immune activation often
             involve maternal administration of agents that activate
             toll-like receptors (TLRs), a class of pattern recognition
             receptors that initiate innate immune responses. Such
             studies have focused primarily on activating the TLR3 or
             TLR4 subtypes, to mimic immune responses to viral or
             bacterial infections, respectively. Here, we characterize
             the effects of prenatal activation of TLR7, which is
             implicated in the pathogenesis of autoimmune disease.
             Prenatal TLR7 activation via administration of the selective
             agonist imiquimod (5.0 mg/kg) induces a phenotype in
             offspring characterized by reduced anxiety-like behavior,
             fragmented social behavior, and altered ultrasonic
             vocalization patterns at 6-12 weeks of age. The
             characteristics of this phenotype are readily
             distinguishable from-and in some ways opposite to-those seen
             following prenatal activation of TLR3 and/or TLR4. Prenatal
             TLR7-activated mice have normal baseline locomotor activity,
             but are hyperresponsive to stimuli including social
             partners, circadian cues, and gonadal hormone fluctuations.
             These alterations are accompanied by decreases in microglia
             density but increases in ramifications. RNA-sequencing of
             dorsal striatum, a region showing profound changes in
             microglial markers, indicates that prenatal TLR7 activation
             induces differential expression of hundreds of genes at 13
             weeks of age, with virtually no overlap in differentially
             expressed genes between males and females. Our findings
             demonstrate that prenatal immune activation can promote a
             wide range of developmental trajectories, depending on the
             type and/or pattern of TLR activation and the sex of the
             offspring.},
   Doi = {10.1038/s41380-018-0346-4},
   Key = {fds340827}
}

@article{fds339552,
   Author = {Kentner, AC and Bilbo, SD and Brown, AS and Hsiao, EY and McAllister,
             AK and Meyer, U and Pearce, BD and Pletnikov, MV and Yolken, RH and Bauman,
             MD},
   Title = {Maternal immune activation: reporting guidelines to improve
             the rigor, reproducibility, and transparency of the
             model.},
   Journal = {Neuropsychopharmacology},
   Volume = {44},
   Number = {2},
   Pages = {245-258},
   Year = {2019},
   Month = {January},
   url = {http://dx.doi.org/10.1038/s41386-018-0185-7},
   Abstract = {The 2017 American College of Neuropychopharmacology (ACNP)
             conference hosted a Study Group on 4 December 2017,
             Establishing best practice guidelines to improve the rigor,
             reproducibility, and transparency of the maternal immune
             activation (MIA) animal model of neurodevelopmental
             abnormalities. The goals of this session were to (a)
             evaluate the current literature and establish a consensus on
             best practices to be implemented in MIA studies, (b)
             identify remaining research gaps warranting additional data
             collection and lend to the development of evidence-based
             best practice design, and (c) inform the MIA research
             community of these findings. During this session, there was
             a detailed discussion on the importance of validating
             immunogen doses and standardizing the general design (e.g.,
             species, immunogenic compound used, housing) of our MIA
             models both within and across laboratories. The consensus of
             the study group was that data does not currently exist to
             support specific evidence-based model selection or
             methodological recommendations due to lack of consistency in
             reporting, and that this issue extends to other inflammatory
             models of neurodevelopmental abnormalities. This launched a
             call to establish a reporting checklist focusing on
             validation, implementation, and transparency modeled on the
             ARRIVE Guidelines and CONSORT (scientific reporting
             guidelines for animal and clinical research, respectively).
             Here we provide a summary of the discussions in addition to
             a suggested checklist of reporting guidelines needed to
             improve the rigor and reproducibility of this valuable
             translational model, which can be adapted and applied to
             other animal models as well.},
   Doi = {10.1038/s41386-018-0185-7},
   Key = {fds339552}
}

@article{fds339550,
   Author = {Bordt, EA and Smith, CJ and Demarest, TG and Bilbo, SD and Kingsbury,
             MA},
   Title = {Mitochondria, Oxytocin, and Vasopressin: Unfolding the
             Inflammatory Protein Response.},
   Journal = {Neurotoxicity Research},
   Year = {2018},
   Month = {September},
   url = {http://dx.doi.org/10.1007/s12640-018-9962-7},
   Abstract = {Neuroendocrine and immune signaling pathways are activated
             following insults such as stress, injury, and infection, in
             a systemic response aimed at restoring homeostasis.
             Mitochondrial metabolism and function have been implicated
             in the control of immune responses. Commonly studied along
             with mitochondrial function, reactive oxygen species (ROS)
             are closely linked to cellular inflammatory responses. It is
             also accepted that cells experiencing mitochondrial or
             endoplasmic reticulum (ER) stress induce response pathways
             in order to cope with protein-folding dysregulation, in
             homeostatic responses referred to as the unfolded protein
             responses (UPRs). Recent reports indicate that the UPRs may
             play an important role in immune responses. Notably, the
             homeostasis-regulating hormones oxytocin (OXT) and
             vasopressin (AVP) are also associated with the regulation of
             inflammatory responses and immune function. Intriguingly,
             OXT and AVP have been linked with ER unfolded protein
             responses (UPRER), and can impact ROS production and
             mitochondrial function. Here, we will review the evidence
             for interactions between these various factors and how these
             neuropeptides might influence mitochondrial
             processes.},
   Doi = {10.1007/s12640-018-9962-7},
   Key = {fds339550}
}

@article{fds339551,
   Author = {Kopec, AM and Smith, CJ and Ayre, NR and Sweat, SC and Bilbo,
             SD},
   Title = {Microglial dopamine receptor elimination defines
             sex-specific nucleus accumbens development and social
             behavior in adolescent rats.},
   Journal = {Nature Communications},
   Volume = {9},
   Number = {1},
   Pages = {3769},
   Year = {2018},
   Month = {September},
   url = {http://dx.doi.org/10.1038/s41467-018-06118-z},
   Abstract = {Adolescence is a developmental period in which the
             mesolimbic dopaminergic "reward" circuitry of the brain,
             including the nucleus accumbens (NAc), undergoes significant
             plasticity. Dopamine D1 receptors (D1rs) in the NAc are
             critical for social behavior, but how these receptors are
             regulated during adolescence is not well understood. In this
             report, we demonstrate that microglia and
             complement-mediated phagocytic activity shapes NAc
             development by eliminating D1rs in male, but not female
             rats, during adolescence. Moreover, immune-mediated
             elimination of D1rs is required for natural developmental
             changes in male social play behavior. These data demonstrate
             for the first time that microglia and complement-mediated
             immune signaling (i) participate in adolescent brain
             development in a sex-specific manner, and (ii) are causally
             implicated in developmental changes in behavior. These data
             have broad implications for understanding the adolescent
             critical period of development, the molecular mechanisms
             underlying social behavior, and sex differences in brain
             structure and function.},
   Doi = {10.1038/s41467-018-06118-z},
   Key = {fds339551}
}

@article{fds339553,
   Author = {Bilbo, SD},
   Title = {The diverse culinary habits of microglia.},
   Journal = {Nature Neuroscience},
   Volume = {21},
   Number = {8},
   Pages = {1023-1025},
   Year = {2018},
   Month = {August},
   url = {http://dx.doi.org/10.1038/s41593-018-0196-z},
   Doi = {10.1038/s41593-018-0196-z},
   Key = {fds339553}
}

@article{fds339554,
   Author = {Kopec, AM and Fiorentino, MR and Bilbo, SD},
   Title = {Gut-immune-brain dysfunction in Autism: Importance of
             sex.},
   Journal = {Brain Research},
   Volume = {1693},
   Number = {Pt B},
   Pages = {214-217},
   Year = {2018},
   Month = {August},
   url = {http://dx.doi.org/10.1016/j.brainres.2018.01.009},
   Abstract = {Autism Spectrum Disorder (ASD) is characterized by social
             behavior deficits, stereotypies, cognitive rigidity, and in
             some cases severe intellectual impairment and developmental
             delay. Although ASD is most widely identified by its
             neurological deficits, gastrointestinal issues are common in
             ASD. An intimate and complex relationship exists between the
             gut, the immune system, and the brain, leading to the
             hypothesis that ASD may be a systems-level disease affecting
             the gut and immune systems, in addition to the brain.
             Despite significant advances in understanding the
             contribution of the gut and immune systems to the etiology
             of ASD, there is an intriguing commonality among patients
             that is not well understood: they are predominantly male.
             Virtually no attention has been given to the potential role
             of sex-specific regulation of gut, peripheral, and central
             immune function in ASD, despite the 4:1 male-to-female bias
             in this disorder. In this review, we discuss recent
             revelations regarding the impact of gut-immune-brain
             relationships on social behavior in rodent models and in ASD
             patients, placing them in the context of known or putative
             sex specific mechanisms.},
   Doi = {10.1016/j.brainres.2018.01.009},
   Key = {fds339554}
}

@article{fds339722,
   Author = {Bilbo, SD},
   Title = {Sex Differences Shape Brain Development and Function, in
             Health and Disease: Policy Implications},
   Journal = {Policy Insights From the Behavioral and Brain
             Sciences},
   Volume = {5},
   Number = {1},
   Pages = {104-109},
   Publisher = {SAGE Publications},
   Year = {2018},
   Month = {March},
   url = {http://dx.doi.org/10.1177/2372732217742673},
   Abstract = {© The Author(s) 2017. Sex differences profoundly impact
             health and disease. Despite this, the inclusion of females
             in clinical and fundamental research lags far behind
             advances in other aspects of medicine, especially in the
             brain sciences. Regardless of whether neuroscientists are
             intrinsically interested in sex differences per se,
             observing a sex disparity in the incidence or presentation
             of a given neurological disorder provides a significant clue
             into the neurobiology of that disorder. Autism spectrum
             disorder (ASD) is one of the most sex-biased disorders, with
             a 4:1 male-to-female ratio, an important aspect of its
             etiology and biology that has largely been ignored in the
             preclinical literature. This article briefly overviews what
             is known about the sexual differentiation of the developing
             healthy brain, with a focus on the preclinical literature.
             This places observed sex differences in neurological
             disorders such as ASD into the context of known sex
             differences in neurobiology—along with insight from known
             sex-specific mechanisms in other systems that impact the
             brain (e.g., immune system, microbiome). Finally, the
             article provides recommendations for progress
             forward.},
   Doi = {10.1177/2372732217742673},
   Key = {fds339722}
}

@article{fds342607,
   Author = {Hanamsagar, R and Alter, MD and Block, CS and Sullivan, H and Bolton,
             JL and Bilbo, SD},
   Title = {Generation of a microglial developmental index in mice and
             in humans reveals a sex difference in maturation and immune
             reactivity.},
   Journal = {Glia},
   Volume = {66},
   Number = {2},
   Pages = {460},
   Year = {2018},
   Month = {February},
   url = {http://dx.doi.org/10.1002/glia.23277},
   Doi = {10.1002/glia.23277},
   Key = {fds342607}
}

@article{fds339555,
   Author = {Bilbo, SD and Block, CL and Bolton, JL and Hanamsagar, R and Tran,
             PK},
   Title = {Beyond infection - Maternal immune activation by
             environmental factors, microglial development, and relevance
             for autism spectrum disorders.},
   Journal = {Experimental Neurology},
   Volume = {299},
   Number = {Pt A},
   Pages = {241-251},
   Year = {2018},
   Month = {January},
   url = {http://dx.doi.org/10.1016/j.expneurol.2017.07.002},
   Abstract = {Immune molecules such as cytokines and chemokines and the
             cells that produce them within the brain, notably microglia,
             are critical for normal brain development. This recognition
             has in recent years led to the working hypothesis that
             inflammatory events during pregnancy, e.g. in response to
             infection, may disrupt the normal expression of immune
             molecules during critical stages of neural development and
             thereby contribute to the risk for neurodevelopmental
             disorders such as autism spectrum disorder (ASD). This
             hypothesis has in large part been shepherded by the work of
             Dr. Paul Patterson and colleagues, which has elegantly
             demonstrated that a single viral infection or injection of a
             viral mimetic to pregnant mice significantly and
             persistently impacts offspring immune and nervous system
             function, changes that underlie ASD-like behavioral
             dysfunction including social and communication deficits.
             Subsequent studies by many labs - in humans and in non-human
             animal models - have supported the hypothesis that ongoing
             disrupted immune molecule expression and/or
             neuroinflammation contributes to at least a significant
             subset of ASD. The heterogeneous clinical and biological
             phenotypes observed in ASD strongly suggest that in
             genetically susceptible individuals, environmental risk
             factors combine or synergize to create a tipping or
             threshold point for dysfunction. Importantly, animal studies
             showing a link between maternal immune activation (MIA) and
             ASD-like outcomes in offspring involve different species and
             diverse environmental factors associated with ASD in humans,
             beyond infection, including toxin exposures, maternal
             stress, and maternal obesity, all of which impact
             inflammatory or immune pathways. The goal of this review is
             to highlight the broader implications of Dr. Patterson's
             work for the field of autism, with a focus on the impact
             that MIA by diverse environmental factors has on fetal brain
             development, immune system development, and the
             pathophysiology of ASD.},
   Doi = {10.1016/j.expneurol.2017.07.002},
   Key = {fds339555}
}

@article{fds340068,
   Author = {Edlow, AG and Glass, RM and Smith, CJ and Tran, PK and James, K and Bilbo,
             S},
   Title = {Placental Macrophages: A Window Into Fetal Microglial
             Function in Maternal Obesity},
   Journal = {International Journal of Developmental Neuroscience : the
             Official Journal of the International Society for
             Developmental Neuroscience},
   Publisher = {Elsevier BV},
   Year = {2018},
   Month = {January},
   url = {http://dx.doi.org/10.1016/j.ijdevneu.2018.11.004},
   Abstract = {© 2018 ISDN Fetal placental macrophages and microglia
             (resident brain macrophages) have a common origin in the
             fetal yolk sac. Yolk-sac-derived macrophages comprise the
             permanent pool of brain microglia throughout an individual's
             lifetime. Inappropriate fetal microglial priming may
             therefore have lifelong neurodevelopmental consequences, but
             direct evaluation of microglial function in a living fetus
             or neonate is impossible. We sought to test the hypothesis
             that maternal obesity would prime both placental macrophages
             and fetal brain microglia to overrespond to an immune
             challenge, thus providing a window into microglial function
             using placental cells. Obesity was induced in C57BL/6 J mice
             using a 60% high-fat diet. On embryonic day 17.5, fetal
             brain microglia and corresponding CD11b + placental cells
             were isolated from fresh tissue. Cells were treated with
             media or lipopolysaccharide (LPS). Tumor necrosis
             factor-alpha (TNF-α) production by stimulated and
             unstimulated cells was quantified via ELISA. We demonstrate
             for the first time that the proinflammatory cytokine
             production of CD11b + placental cells is strongly correlated
             with that of brain microglia (Spearman's ρ = 0.73, p =
             0.002) in the setting of maternal obesity. Maternal
             obesity-exposed CD11b + cells had an exaggerated response to
             LPS compared to controls, with a 5.1-fold increase in TNF-α
             production in placentas (p = 0.003) and 3.8-fold increase in
             TNF-α production in brains (p = 0.002). In sex-stratified
             analyses, only male obesity-exposed brains and placentas had
             significant increase in TNF-α production in response to
             LPS. Taken together, these data suggest that maternal
             obesity primes both placental macrophages and fetal brain
             microglia to overproduce a proinflammatory cytokine in
             response to immune challenge. Male brain and placental
             immune response is more marked than female in this setting.
             Given that fetal microglial priming may impact neuroimmune
             function throughout the lifespan, these data could provide
             insight into the male predominance of certain
             neurodevelopmental morbidities linked to maternal obesity,
             including cognitive dysfunction, autism spectrum disorder,
             and ADHD. Placental CD11b+ macrophages may have the
             potential to serve as an accessible biomarker of aberrant
             fetal brain immune activation in maternal obesity. This
             finding may have broader implications for assaying the
             impact of other maternal exposures on fetal brain
             development.},
   Doi = {10.1016/j.ijdevneu.2018.11.004},
   Key = {fds340068}
}

@article{fds339556,
   Author = {Hanamsagar, R and Bilbo, SD},
   Title = {Environment matters: microglia function and dysfunction in a
             changing world.},
   Journal = {Current Opinion in Neurobiology},
   Volume = {47},
   Pages = {146-155},
   Year = {2017},
   Month = {December},
   url = {http://dx.doi.org/10.1016/j.conb.2017.10.007},
   Abstract = {The immune system is our interface with the environment, and
             immune molecules such as cytokines and chemokines and the
             cells that produce them within the brain, notably microglia,
             are critical for normal brain development. This recognition
             has in recent years led to the working hypothesis that
             inflammatory events during pregnancy or the early postnatal
             period, for example, in response to infection, may disrupt
             the normal developmental trajectory of microglia and
             consequently their interactions with neurons, thereby
             contributing to the risk for neurological disorders. The
             current article outlines recent findings on the impact of
             diverse, pervasive environmental challenges, beyond
             infection, including air pollution and maternal stress; and
             their impact on microglial development and its broad
             implications for neural pathologies.},
   Doi = {10.1016/j.conb.2017.10.007},
   Key = {fds339556}
}

@article{fds339557,
   Author = {Hanamsagar, R and Alter, MD and Block, CS and Sullivan, H and Bolton,
             JL and Bilbo, SD},
   Title = {Generation of a microglial developmental index in mice and
             in humans reveals a sex difference in maturation and immune
             reactivity.},
   Journal = {Glia},
   Volume = {65},
   Number = {9},
   Pages = {1504-1520},
   Year = {2017},
   Month = {September},
   url = {http://dx.doi.org/10.1002/glia.23176},
   Abstract = {Evidence suggests many neurological disorders emerge when
             normal neurodevelopmental trajectories are disrupted, i.e.,
             when circuits or cells do not reach their fully mature
             state. Microglia play a critical role in normal
             neurodevelopment and are hypothesized to contribute to brain
             disease. We used whole transcriptome profiling with Next
             Generation sequencing of purified developing microglia to
             identify a microglial developmental gene expression program
             involving thousands of genes whose expression levels change
             monotonically (up or down) across development. Importantly,
             the gene expression program was delayed in males relative to
             females and exposure of adult male mice to LPS, a potent
             immune activator, accelerated microglial development in
             males. Next, a microglial developmental index (MDI)
             generated from gene expression patterns obtained from
             purified mouse microglia, was applied to human brain
             transcriptome datasets to test the hypothesis that
             variability in microglial development is associated with
             human diseases such as Alzheimer's and autism where
             microglia have been suggested to play a role. MDI was
             significantly increased in both Alzheimer's Disease and in
             autism, suggesting that accelerated microglial development
             may contribute to neuropathology. In conclusion, we
             identified a microglia-specific gene expression program in
             mice that was used to create a microglia developmental
             index, which was applied to human datasets containing
             heterogeneous cell types to reveal differences between
             healthy and diseased brain samples, and between males and
             females. This powerful tool has wide ranging applicability
             to examine microglial development within the context of
             disease and in response to other variables such as stress
             and pharmacological treatments.},
   Doi = {10.1002/glia.23176},
   Key = {fds339557}
}

@article{fds197406,
   Author = {SD Bilbo and NJ Newsum and DB Sprunger and LR Watkins and JW Rudy and SF
             Maier},
   Title = {Differential effects of neonatal handling on early life
             infection-induced alterations in cognition in
             adulthood.},
   Journal = {Brain, behavior, and immunity},
   Volume = {21},
   Number = {3},
   Pages = {332-42},
   Year = {2007},
   Month = {March},
   ISSN = {0889-1591},
   url = {http://dx.doi.org/10.1016/j.bbi.2006.10.005},
   Keywords = {Age Factors • Analysis of Variance • Animals
             • Animals, Newborn • Bacterial Infections •
             Behavior, Animal • Cognition • Critical Period
             (Psychology) • Fear • Female • Handling
             (Psychology) • Hippocampus • Interleukin-10 •
             Learning • Lipopolysaccharides • Male •
             Neuroglia • Neuroimmunomodulation • Rats •
             Rats, Sprague-Dawley • Stress, Psychological •
             immunology • immunology* • metabolism •
             physiology • physiology*},
   Abstract = {We have previously demonstrated that bacterial infection
             (Escherichia coli) in neonatal rats is associated with
             impaired memory in a fear-conditioning task in adulthood.
             This impairment, however, is only observed if a peripheral
             immune challenge (lipopolysaccharide; LPS) is administered
             around the time of learning. We used a brief
             separation/handling paradigm to determine if the adult
             memory impairment associated with neonatal-infection could
             be prevented. Naturally occurring variations in maternal
             care promote striking variations in offspring cognitive
             development, and handling paradigms are used to manipulate
             the quality and quantity of maternal care. Rats were
             injected on post natal (P) day 4 with E. coli or PBS, and
             half from each group were handled for 15 min/day from P4 to
             20. All rats were then tested in adulthood. Neonatal
             handling of rats infected as neonates prevented the increase
             in microglial cell marker reactivity within the hippocampus,
             and the exaggerated brain IL-1beta production to LPS
             normally produced by the infection. Thus, these neural
             processes were now comparable to levels of non-infected PBS
             controls. Furthermore, handling completely prevented
             LPS-induced memory impairment in a context-fear task in
             adult rats infected as neonates. Finally, neonatal handling
             dramatically improved spatial learning and memory and
             decreased anxiety in rats treated early with PBS, but had no
             beneficial effect on these measures in rats infected as
             neonates. Taken together, these data suggest that maternal
             care may profoundly influence neuroinflammatory processes in
             adulthood, and that infection may also prevent maternal care
             influences on cognition later in life.},
   Language = {eng},
   Doi = {10.1016/j.bbi.2006.10.005},
   Key = {fds197406}
}

@article{fds197407,
   Author = {SD Bilbo and JW Rudy and LR Watkins and SF Maier},
   Title = {A behavioural characterization of neonatal
             infection-facilitated memory impairment in adult
             rats.},
   Journal = {Behavioural brain research},
   Volume = {169},
   Number = {1},
   Pages = {39-47},
   Year = {2006},
   Month = {April},
   ISSN = {0166-4328},
   url = {http://dx.doi.org/10.1016/j.bbr.2005.12.002},
   Keywords = {Age Factors • Amnesia, Retrograde • Animals •
             Animals, Newborn • Association Learning •
             Bacterial Infections • Behavior, Animal •
             Conditioning, Classical • Critical Period (Psychology)
             • Disease Models, Animal • Fear • Female
             • Hippocampus • Lipopolysaccharides • Male
             • Rats • Rats, Sprague-Dawley • complications
             • etiology • immunology • immunology* •
             physiology • physiology* • physiopathology},
   Abstract = {We have reported that exposure to bacteria (Escherichia
             coli) during the neonatal period in rats is associated with
             impaired memory for a novel context in adulthood. However,
             impairment is only observed if a peripheral immune challenge
             (bacterial lipopolysaccharide (LPS)) is administered
             immediately following context exposure. The goal of the
             current study was to more fully characterize this
             phenomenon. In Experiment 1, memory impairment as a result
             of neonatal infection and subsequent LPS challenge was
             observed in juvenile rats, indicating that the changes
             induced by infection occur early on and are then manifest
             throughout the lifespan. In Experiment 2, infection in
             juvenile rats did not lead to LPS-induced memory impairment
             in adulthood, suggesting there is a critical period for
             early infection-induced alterations. In Experiments 3 and 4,
             memory for a novel context was impaired in neonatally
             infected rats, a task that is dependent on the hippocampus,
             whereas cued memory for a tone, which does not depend on the
             hippocampus, was not impaired. Furthermore, long-term, but
             not short-term contextual memory was impaired in adult rats
             infected as neonates following an LPS challenge either 24 h
             before or immediately after conditioning. Finally, in
             Experiment 5, no neonatal group differences were observed in
             corticosterone or open field behaviour, suggesting that
             decreased freezing to a conditioned context reflects
             impaired memory, and not simply hyperactivity or altered
             stress reactivity. Taken together, we have demonstrated that
             neonatal infection results in robust hippocampal-dependent
             memory impairment following an immune challenge in adulthood
             using a number of conditioning paradigms.},
   Language = {eng},
   Doi = {10.1016/j.bbr.2005.12.002},
   Key = {fds197407}
}

@article{fds197409,
   Author = {GN Neigh and ER Glasper and SD Bilbo and RJ Traystman and A Courtney
             DeVries},
   Title = {Cardiac arrest/cardiopulmonary resuscitation augments
             cell-mediated immune function and transiently suppresses
             humoral immune function.},
   Journal = {Journal of cerebral blood flow and metabolism : official
             journal of the International Society of Cerebral Blood Flow
             and Metabolism},
   Volume = {25},
   Number = {11},
   Pages = {1424-32},
   Year = {2005},
   Month = {November},
   ISSN = {0271-678X},
   url = {http://dx.doi.org/10.1038/sj.jcbfm.9600137},
   Keywords = {Animals • Antibody Formation • Antigens •
             Cardiopulmonary Resuscitation* • Corticosterone •
             Heart Arrest • Hippocampus • Humans •
             Hypersensitivity, Delayed • Hypothalamo-Hypophyseal
             System • Hypothermia • Immunity, Cellular •
             Ischemia • Male • Mice • Neurons •
             Pituitary-Adrenal System • blood • immunology
             • immunology* • injuries • metabolism •
             methods • prevention & control •
             therapy},
   Abstract = {Immune system activation has implications for
             cerebrovascular health, but little is known about the
             function of the immune system after a major cerebrovascular
             event, such as cardiac arrest and cardiopulmonary
             resuscitation (CA/CPR). Cardiac arrest and cardiopulmonary
             resuscitation damages the hippocampus, an important
             component of the hypothalamic-pituitary-adrenal (HPA) axis,
             and alterations in HPA axis activity can affect immune
             function. We tested the hypothesis that CA/CPR
             (approximately 8 mins) would cause HPA axis dysregulation
             and alter the delayed type hypersensitivity (DTH) response
             to antigenic challenge. We also assessed the primary and
             secondary antibody response of mice exposed to CA/CPR. Of
             the mice exposed to CA/CPR, half had brains protected by
             hypothermia to isolate the effects of the CA/CPR procedure
             from the effects of CA/CPR-induced neuronal damage. Cardiac
             arrest and cardiopulmonary resuscitation-induced neuronal
             damage resulted in a persistent elevation of blood
             corticosterone concentration and a concomitant augmentation
             of the DTH response to antigenic challenge. Furthermore,
             immune activation before CA/CPR decreased survival after
             global ischemia. These data highlight the potential impact
             of neuronal damage on cell-mediated immune function and the
             role of humoral immune activation in outcome after global
             ischemia.},
   Language = {eng},
   Doi = {10.1038/sj.jcbfm.9600137},
   Key = {fds197409}
}

@article{fds197408,
   Author = {SD Bilbo and JC Biedenkapp and A Der-Avakian and LR Watkins and JW Rudy and SF Maier},
   Title = {Neonatal infection-induced memory impairment after
             lipopolysaccharide in adulthood is prevented via caspase-1
             inhibition.},
   Journal = {The Journal of neuroscience : the official journal of the
             Society for Neuroscience},
   Volume = {25},
   Number = {35},
   Pages = {8000-9},
   Year = {2005},
   Month = {August},
   ISSN = {1529-2401},
   url = {http://dx.doi.org/10.1523/JNEUROSCI.1748-05.2005},
   Keywords = {Age Factors • Animals • Animals, Newborn •
             Caspase 1 • Enzyme Inhibitors • Escherichia coli
             Infections • Female • Hippocampus •
             Interleukin-1 • Lipopolysaccharides • Male •
             Memory Disorders • Pregnancy • Rats • Rats,
             Sprague-Dawley • antagonists & inhibitors •
             antagonists & inhibitors* • chemically induced •
             drug effects • drug therapy • enzymology •
             enzymology* • metabolism • microbiology •
             pharmacology • physiology • prevention & control*
             • therapeutic use* • toxicity*},
   Abstract = {We have reported that neonatal infection leads to memory
             impairment after an immune challenge in adulthood. Here we
             explored whether events occurring as a result of early
             infection alter the response to a subsequent immune
             challenge in adult rats, which may then impair memory. In
             experiment 1, peripheral infection with Escherichia coli on
             postnatal day 4 increased cytokines and corticosterone in
             the periphery, and cytokine and microglial cell marker gene
             expression in the hippocampus of neonate pups. Next, rats
             treated neonatally with E. coli or PBS were injected in
             adulthood with lipopolysaccharide (LPS) or saline and killed
             1-24 h later. Microglial cell marker mRNA was elevated in
             hippocampus in saline controls infected as neonates.
             Furthermore, LPS induced a greater increase in glial cell
             marker mRNA in hippocampus of neonatally infected rats, and
             this increase remained elevated at 24 h versus controls.
             After LPS, neonatally infected rats exhibited faster
             increases in interleukin-1beta (IL-1beta) within the
             hippocampus and cortex and a prolonged response within the
             cortex. There were no group differences in peripheral
             cytokines or corticosterone. In experiment 2, rats treated
             neonatally with E. coli or PBS received as adults either
             saline or a centrally administered caspase-1 inhibitor,
             which specifically prevents the synthesis of IL-1beta, 1 h
             before a learning event and subsequent LPS challenge.
             Caspase-1 inhibition completely prevented LPS-induced memory
             impairment in neonatally infected rats. These data implicate
             IL-1beta in the set of immune/inflammatory events that occur
             in the brain as a result of neonatal infection, which likely
             contribute to cognitive alterations in adulthood.},
   Language = {eng},
   Doi = {10.1523/JNEUROSCI.1748-05.2005},
   Key = {fds197408}
}

@article{fds197410,
   Author = {SD Bilbo and LH Levkoff and JH Mahoney and LR Watkins and JW Rudy and SF
             Maier},
   Title = {Neonatal infection induces memory impairments following an
             immune challenge in adulthood.},
   Journal = {Behavioral neuroscience},
   Volume = {119},
   Number = {1},
   Pages = {293-301},
   Year = {2005},
   Month = {February},
   ISSN = {0735-7044},
   url = {http://dx.doi.org/10.1037/0735-7044.119.1.293},
   Keywords = {Animals • Astrocytes • Escherichia coli •
             Escherichia coli Infections • Female • Hippocampus
             • Interleukin-1 • Lipopolysaccharides • Male
             • Memory Disorders • Pregnancy • Pregnancy
             Complications, Infectious • Prenatal Exposure Delayed
             Effects* • Rats • analysis • complications*
             • immunology • immunology* • pathogenicity*
             • pathology* • pharmacology • physiology
             • physiopathology* • poisoning • psychology*
             • veterinary},
   Abstract = {Exposure to infectious agents during early postnatal life
             often alters glucocorticoid responses to stress and immune
             outcomes in adulthood. The authors examined whether neonatal
             infection results in memory impairments in adult animals.
             Rats infected with Escherichia coli (E. coli) as neonates
             displayed impaired memory for a recently explored context in
             adulthood. This impairment, however, was only observed in
             rats that received a peripheral immune challenge
             (lipopolysaccharide; LPS) immediately following context
             exposure. Adult rats treated neonatally with E. coli also
             had decreased hippocampal astrocytes compared with
             phosphate-buffered saline-treated rats, but displayed
             increased astrocyte reactivity in the hippocampus and
             decreased brain interleukin-1beta following
             lipopolysaccharide. Infection during development appears to
             alter glia within the hippocampus, which may contribute to
             altered cytokine responses and memory impairment.},
   Language = {eng},
   Doi = {10.1037/0735-7044.119.1.293},
   Key = {fds197410}
}

@article{fds197411,
   Author = {BJ Prendergast and SD Bilbo and RJ Nelson},
   Title = {Short day lengths enhance skin immune responses in
             gonadectomised Siberian hamsters.},
   Journal = {Journal of neuroendocrinology},
   Volume = {17},
   Number = {1},
   Pages = {18-21},
   Year = {2005},
   Month = {January},
   ISSN = {0953-8194},
   url = {http://dx.doi.org/10.1111/j.1365-2826.2005.01273.x},
   Keywords = {Androgens • Animals • Cricetinae •
             Hypersensitivity, Delayed • Immune System • Male
             • Orchiectomy • Periodicity • Phodopus •
             Photoperiod* • Skin • Testosterone • drug
             effects • immunology* • pharmacology* •
             physiology • physiopathology*},
   Abstract = {In Siberian hamsters and other photoperiodic rodents,
             exposure to short photoperiods simultaneously inhibits
             gonadal hormone secretion and enhances some measures of
             immune function. The present study tested whether gonadal
             hormones mediate the effects of short days on skin immune
             function (delayed-type hypersensitivity reactions) in male
             Siberian hamsters. The magnitude of delayed-type
             hypersensitivity reactions was greater in hamsters exposed
             to short days relative to those in long days. Comparable
             effects of photoperiod were obtained in castrated hamsters
             bearing empty or testosterone-filled implants. The data
             suggest that contemporary gonadal hormone secretion is
             neither necessary, nor sufficient to mediate the effects of
             short photoperiods on skin immune function.},
   Language = {eng},
   Doi = {10.1111/j.1365-2826.2005.01273.x},
   Key = {fds197411}
}

@article{fds197412,
   Author = {GN Neigh and SD Bilbo and AK Hotchkiss and RJ Nelson},
   Title = {Exogenous pyruvate prevents stress-evoked suppression of
             mitogen-stimulated proliferation.},
   Journal = {Brain, behavior, and immunity},
   Volume = {18},
   Number = {5},
   Pages = {425-33},
   Year = {2004},
   Month = {September},
   ISSN = {0889-1591},
   url = {http://dx.doi.org/10.1016/j.bbi.2003.10.001},
   Keywords = {Analysis of Variance • Animals • Cell Division
             • Corticosterone • Dose-Response Relationship,
             Drug • Down-Regulation • Energy Metabolism •
             Injections, Intraperitoneal • Lactic Acid • Male
             • Mice • Mice, Inbred C57BL • Mitogens •
             Pyruvic Acid • Restraint, Physical • Spleen •
             Stress, Psychological • administration & dosage* •
             blood • cytology* • drug effects • immunology
             • metabolism* • pharmacology • physiology
             • physiology* • physiopathology •
             psychology},
   Abstract = {Although the phenomenon that psychological stress influences
             disease onset and progression is well established, the
             mechanisms underlying stress-evoked compromise of immune
             function remain unspecified. To test the hypothesis that
             energetic shortages compromise immunity, we evaluated the
             effectiveness of pyruvate, a metabolic supplement, to
             prevent stress-evoked suppression of mitogen-stimulated
             splenocyte proliferation. Male C57BL/6 mice were subjected
             to 2h of restraint once daily for 14 days. Consistent with
             previous studies, mitogen-stimulated splenocyte
             proliferation was reduced after restraint; in contrast, mice
             that received pyruvate injections immediately following each
             episode of restraint did not reduce splenocyte
             proliferation. In addition, restraint-evoked corticosterone
             elevation did not habituate in animals treated with
             pyruvate, suggesting that glucocorticoids are not
             exclusively immunosuppressive. The ratio of pyruvate to
             lactate, an index of aerobic metabolism, was elevated in
             mice exposed to restraint suggesting that mice exposed to
             restraint were preferentially using aerobic metabolism and
             producing more ATP per unit of pyruvate than non-restrained
             mice. Furthermore, two of the effective doses of pyruvate
             (0.5 and 500.0mg/kg) altered glucose levels suggesting a
             metabolic function of the supplement. Although several
             different mechanisms could possibly mediate the changes in
             splenocyte proliferation, these results support the
             hypothesis that stress-evoked immunosuppression may be a
             function of metabolic energy shortages and can be prevented
             via pyruvate supplementation.},
   Language = {eng},
   Doi = {10.1016/j.bbi.2003.10.001},
   Key = {fds197412}
}

@article{fds197413,
   Author = {BJ Prendergast and SD Bilbo and FS Dhabhar and RJ
             Nelson},
   Title = {Effects of photoperiod history on immune responses to
             intermediate day lengths in Siberian hamsters (Phodopus
             sungorus).},
   Journal = {Journal of neuroimmunology},
   Volume = {149},
   Number = {1-2},
   Pages = {31-9},
   Year = {2004},
   Month = {April},
   ISSN = {0165-5728},
   url = {http://dx.doi.org/10.1016/j.jneuroim.2003.12.006},
   Keywords = {Age Factors • Analysis of Variance • Animals
             • Animals, Newborn • Behavior, Animal • Body
             Weight • Cricetinae • Dinitrobenzenes •
             Environment • Enzyme-Linked Immunosorbent Assay •
             Female • Hair • Hemocyanin • Immune System
             • Immunization • Immunoglobulins • Leukocyte
             Count • Leukocytes • Lymphocyte Activation •
             Male • Organ Size • Phodopus • Photoperiod*
             • Pregnancy • Seasons* • Testis • Time
             Factors • blood • immunology • immunology*
             • metabolism • methods • pharmacology •
             physiology • radiation effects • radiation
             effects*},
   Abstract = {Seasonal changes in day length enhance or suppress immune
             function in individuals of several mammalian species.
             Siberian hamsters (Phodopus sungorus) are long-day breeders
             that adjust reproductive physiology and behavior, body mass,
             and immune function following exposure to short
             photoperiods. Photoperiods of intermediate-duration,
             encountered in nature by juvenile hamsters born in
             early-spring and by those born in mid-summer, trigger
             gonadal development in the former cohort and inhibit the
             onset of puberty in the latter. Divergent reproductive
             responses to the same intermediate photoperiod depend on a
             photoperiod history, communicated during gestation. These
             experiments assessed whether photoperiod history during
             gestation likewise impacts immunological responses to
             intermediate photoperiods. Male hamsters were gestated in
             long photoperiods and remained in long photoperiods
             postnatally, or were transferred to an intermediate-duration
             or a short-duration photoperiod; other males were gestated
             in short days and transferred to an intermediate-duration
             photoperiod at birth. Long days stimulated, and short days
             inhibited, somatic and reproductive development;
             intermediate day lengths either accelerated or inhibited
             somatic and reproductive development, depending on whether
             hamsters were gestated in short days or long days,
             respectively. By contrast, photoperiod during gestation did
             not affect most immune endpoints. The data suggest that
             photoperiodic mechanisms that enhance and suppress several
             aspects of immunity in young-adult hamsters are not
             responsive to prenatally communicated photoperiod history
             information.},
   Language = {eng},
   Doi = {10.1016/j.jneuroim.2003.12.006},
   Key = {fds197413}
}

@article{fds197414,
   Author = {BJ Prendergast and AK Hotchkiss and SD Bilbo and RJ
             Nelson},
   Title = {Peripubertal immune challenges attenuate reproductive
             development in male Siberian hamsters (Phodopus
             sungorus).},
   Journal = {Biology of reproduction},
   Volume = {70},
   Number = {3},
   Pages = {813-20},
   Year = {2004},
   Month = {March},
   ISSN = {0006-3363},
   url = {http://dx.doi.org/10.1095/biolreprod.103.023408},
   Keywords = {Animals • Body Temperature • Body Weight •
             Cricetinae • Eating • Female • Hemocyanin
             • Immunoglobulin G • Immunoglobulin M • Male
             • Phodopus • Photoperiod* • Reproduction
             • Sexual Maturation • Testosterone • blood
             • immunology • immunology*},
   Abstract = {Differential allocation of energy to reproduction versus
             host defense is assumed to drive the seasonal antiphase
             relation between peak reproductive function and
             immunocompetence; however, evidence supporting this
             assumption is only correlational. These experiments tested
             whether photoperiod affects immune responses to antigens in
             peripubertal Siberian hamsters, whether such activation of
             the immune system exacts energetic and reproductive costs,
             and whether such costs vary seasonally. Male Siberian
             hamsters were raised from birth in long (LD) or short days
             (SD), which respectively initiate or inhibit the onset of
             puberty. To elicit a specific immune response, hamsters were
             injected with a novel antigen (keyhole limpet hemocyanin
             [KLH]) as juveniles. Reproductive development was attenuated
             and body temperature was elevated in LD hamsters relative to
             saline-injected control animals. In contrast, KLH treatments
             affected neither thermoregulation nor reproductive
             development in photoinhibited SD hamsters. In experiment 2,
             juvenile male hamsters were challenged with bacterial
             lipopolysaccharide (LPS) in order to elicit an innate immune
             response. Febrile and anorexic responses to LPS were greater
             in reproductively stimulated LD hamsters relative to
             reproductively inhibited SD hamsters. LPS treatments
             attenuated somatic and testicular development in LD
             hamsters, but did not significantly affect circulating
             testosterone concentrations. In contrast, LPS treatments
             were without effect on somatic and reproductive development
             in SD hamsters. These experiments indicate that photoperiod
             affects antigen-specific antibody production, febrile
             responses to LPS, and sickness behaviors in juvenile
             Siberian hamsters, and that peripubertal activation of the
             immune system exacts energetic and metabolic costs that can
             diminish the magnitude of somatic and reproductive
             maturation in LD. The data also underscore the importance of
             seasonally dependent life history factors in assessing
             physiological tradeoffs.},
   Language = {eng},
   Doi = {10.1095/biolreprod.103.023408},
   Key = {fds197414}
}

@article{fds197415,
   Author = {SD Bilbo and RJ Nelson},
   Title = {Photoperiod influences the effects of exercise and food
             restriction on an antigen-specific immune response in
             Siberian hamsters.},
   Journal = {Endocrinology},
   Volume = {145},
   Number = {2},
   Pages = {556-64},
   Year = {2004},
   Month = {February},
   ISSN = {0013-7227},
   url = {http://dx.doi.org/10.1210/en.2003-1035},
   Keywords = {Animals • Antigens • Cricetinae • Eating
             • Energy Metabolism • Food Deprivation* •
             Hydrocortisone • Hypersensitivity, Delayed •
             Immunity* • Male • Phodopus • Photoperiod*
             • Physical Exertion • Reproduction • Seasons
             • blood • immunology* • physiology*},
   Abstract = {Environmental conditions influence the onset and severity of
             illness and infection and may compromise survival.
             Energetically challenging conditions during winter may
             directly induce death through hypothermia, starvation, or
             shock. The ability to forecast and prepare for the arrival
             of challenging conditions associated with winter (e.g. low
             temperatures, decreased food) likely confers survival
             advantages. Siberian hamsters (Phodopus sungorus) stop
             reproduction and reduce body mass (approximately 25%) during
             short, winter-like day lengths, resulting in energetic
             savings. Hamsters also increase circulating glucocorticoids
             and lymphocytes (e.g. T cells, NK cells), and exhibit
             enhanced antigen-specific delayed-type-hypersensitivity
             (DTH) responses in the skin during short days (SDs). We
             tested the hypothesis that Siberian hamsters use SD lengths
             to signal the onset of winter to mediate the energetic
             trade-offs among body mass, reproductive function, and
             immune function. Long-day (LD; 16 h light, 8 h dark) and SD
             (8 h light, 16 h dark) hamsters were either food restricted
             (25%) or provided ad libitum (ad lib) food for 4 wk; half of
             all hamsters in each food condition had voluntary access to
             a running wheel, and half remained sedentary. SD hamsters
             enhanced DTH responses compared with LD hamsters under
             sedentary ad lib conditions. Exercise enhanced DTH in LD
             hamsters regardless of food intake. Furthermore,
             food-restriction did not significantly influence DTH in LD
             hamsters. In contrast, food-restriction suppressed DTH in SD
             hamsters regardless of activity condition, and exercise
             modestly enhanced DTH only in SD hamsters with ad lib access
             to food. In sum, moderate energetic deficiency suppressed
             DTH in SD (but not LD) hamsters, and this suggests that
             hamsters may have evolved to enhance immune responses during
             winter in preparation for increased metabolic
             stressors.},
   Language = {eng},
   Doi = {10.1210/en.2003-1035},
   Key = {fds197415}
}

@article{fds197419,
   Author = {BJ Prendergast and SD Bilbo and RJ Nelson},
   Title = {Photoperiod controls the induction, retention, and retrieval
             of antigen-specific immunological memory.},
   Journal = {American journal of physiology. Regulatory, integrative and
             comparative physiology},
   Volume = {286},
   Number = {1},
   Pages = {R54-60},
   Year = {2004},
   Month = {January},
   ISSN = {0363-6119},
   url = {http://dx.doi.org/10.1152/ajpregu.00381.2003},
   Keywords = {Animals • Antibody Formation • Cricetinae •
             Dinitrofluorobenzene • Hemocyanin •
             Hypersensitivity, Delayed • Immunization •
             Immunologic Memory • Male • Phodopus •
             Photoperiod* • Reproduction • immunology* •
             physiology* • physiopathology • radiation effects
             • radiation effects*},
   Abstract = {Changes in day length affect several measures of immunity in
             seasonally breeding mammals. In Siberian hamsters (Phodopus
             sungorus), short day lengths suppress specific secondary
             antibody responses to the keyhole limpet hemocyanin (KLH)
             antigen and enhance cutaneous delayed-type hypersensitivity
             (DTH) responses to dinitrofluorobenzene (DNFB). These
             experiments tested whether day length affects secondary
             antibody and DTH responses by altering immune function
             solely during the interval after the initial exposure to
             each antigen, solely during the interval after the second
             exposure, or during both stages of the respective immune
             responses. Adult male Siberian hamsters were exposed to
             either a long (16 h light/day; LD) or a short (8 h
             light/day; SD) photoperiod for 7.5 wk before receiving an
             initial exposure to each antigen (KLH injection, cutaneous
             DNFB treatment; separate groups of animals for each
             antigen). A subset of LD hamsters was transferred to the SD
             photo-period, and a subset of SD hamsters was transferred to
             the LD photoperiod. Other hamsters remained in LD or SD.
             Eight weeks later, all hamsters were challenged with a
             second subcutaneous injection of KLH or a second application
             of DNFB to the ear, and immune responses were measured.
             Exposure to SD during the primary antibody response did not
             affect secondary IgG responses, but SD exposure during the
             secondary response significantly suppressed IgG production
             independent of day length during the initial KLH treatment.
             In contrast, exposure to SD during the DNFB challenge
             enhanced the ensuing DTH response, but this enhancement
             depended on the photoperiod prevailing during the initial
             exposure. Exposure to SD during the sensitization stage did
             not enhance DTH in hamsters subsequently exposed to LD. The
             data suggest that short photoperiods have enduring effects
             on immune responsiveness and on the establishment and
             retention of immunological memory.},
   Language = {eng},
   Doi = {10.1152/ajpregu.00381.2003},
   Key = {fds197419}
}

@article{fds69264,
   Author = {Bilbo, SD and Hotchkiss, AH and Chiavegatto, S and Nelson,
             RJ},
   Title = {Blunted stress responses in delayed type hypersensitivity in
             mice lacking the neuronal isoform of nitric oxide
             synthase},
   Journal = {Journal of Neuroimmunology},
   Volume = {140},
   Pages = {41-48},
   Year = {2003},
   Key = {fds69264}
}

@article{fds69266,
   Author = {Bilbo, SD and Dhabhar, FS and Viswanathan, K and Light, A and Nelson,
             RJ},
   Title = {Photoperiod affects the expression of sex and species
             differences in leukocyte number and leukocyte trafficking of
             congeneric hamsters},
   Journal = {Psychoneuroendocrinology},
   Volume = {28},
   Number = {8},
   Pages = {1027-1043},
   Year = {2003},
   Key = {fds69266}
}


%% Books   
@book{fds198766,
   Author = {J.M. Schwarz and S.D. Bilbo},
   Title = {The Immune System and the Developing Brain},
   Series = {McCarthy's The Developing Brain Series},
   Publisher = {Morgan and Claypool Life Sciences},
   Year = {2011},
   Key = {fds198766}
}


%% Chapters in Books   
@misc{fds198784,
   Author = {J.M. Schwarz and S.D. Bilbo},
   Title = {Chapter 15: Microglia and Neurodevelopment},
   Booktitle = {The Wiley-Blackwell Handbook of Psychoneuroimmunology},
   Publisher = {Wiley-Blackwell},
   Editor = {Kusnecov and Anisman},
   Year = {2013},
   Month = {December},
   Key = {fds198784}
}


%% Articles Submitted   
@article{fds220606,
   Author = {L.L. Williamson and S.D. Bilbo},
   Title = {Neonatal infection modulates behavioral accuracy and
             hippocampal activation on a Morris Water Maze
             task},
   Journal = {Physiology & Behavior},
   Year = {2013},
   Key = {fds220606}
}


%% Other   
@misc{fds69283,
   Author = {Spataro, LE and Walsh, MG and Levkoff, LH and Wieseler Frank and JL, Frank and MG, Bilbo and SD, Martin and TJ, Maier and SF and Watkins,
             LR},
   Title = {Laparotomy sensitizes dorsal spinal cord glia: Enhanced
             glial response to later challenge},
   Journal = {Society for Neuroscience Abstracts},
   Year = {2004},
   Key = {fds69283}
}

@misc{fds69284,
   Author = {Neigh, GN and Bilbo, SD and Glasper, ER and DeVries,
             AC},
   Title = {Cardiac arrest/cardiopulmonary resuscitation increases the
             delayed-type-hypersensitivity response and alters
             hypothalamic-pituitary adrenal axis activity},
   Journal = {PsychoNeuroImmunology Research Society Abstracts},
   Year = {2004},
   Key = {fds69284}
}

@misc{fds69281,
   Author = {Bilbo, SD and Levkoff, LH and Mahoney, JH and Rudy, JW and Watkins, LR and Maier, SF},
   Title = {Neonatal infection induces memory impairments and cytokine
             alterations following an immune challenge in
             adulthood},
   Journal = {PsychoNeuroImmunology Research Society Abstracts},
   Year = {2004},
   Key = {fds69281}
}

@misc{fds69282,
   Author = {Bilbo, SD and Mahoney, JH and Rudy, JW and Watkins, LR and Maier,
             SF},
   Title = {Neonatal infection alters hippocampal glia and induces
             memory impairments and cytokine alterations following an
             immune challenge in adulthood},
   Journal = {Society for Neuroscience Abstracts},
   Year = {2004},
   Key = {fds69282}
}

@misc{fds69285,
   Author = {Bilbo, SD and Dhabhar, FS and Viswanathan, K and Prendergast, BJ and Nelson, RJ},
   Title = {Sex differences in photoperiodic and stress-induced
             enhancement of immune function in Siberian
             hamsters},
   Journal = {PsychoNeuroImmunology Research Society Abstracts},
   Year = {2003},
   Key = {fds69285}
}

@misc{fds69286,
   Author = {Bilbo, SD and Nelson, RJ},
   Title = {Photoperiod and exercise affect metabolism and delayed type
             hypersensitivity in Siberian hamsters},
   Journal = {Society for Behavioral Neuroendocrinology
             Abstracts},
   Year = {2003},
   Key = {fds69286}
}

@misc{fds69287,
   Author = {Bowers, SL and Bilbo, SD and Nelson, RJ},
   Title = {A comparison of chronic stressors effects on delayed type
             hypersensitivity in mice},
   Journal = {Society for Behavioral Neuroendocrinology
             Abstracts},
   Year = {2003},
   Key = {fds69287}
}

@misc{fds69288,
   Author = {Bilbo, SD and Neigh, GN and Glasper, ER and DeVries,
             AC},
   Title = {Enhanced delayed-type-hypersensitivity responses in cardiac
             arrest survivors},
   Journal = {Society for Neuroscience Abstracts},
   Year = {2003},
   Key = {fds69288}
}

@misc{fds69289,
   Author = {Prendergast, BJ and Bilbo, SD and Nelson, RJ},
   Title = {Day length regulates induction, retention, and retrieval of
             immunological memory in Siberian hamsters},
   Journal = {Society for Neuroscience Abstracts},
   Year = {2003},
   Key = {fds69289}
}

@misc{fds69291,
   Author = {Viswanathan, K and Bilbo, SD and Dhabhar, FS},
   Title = {Acute stress administered before primary immunization or
             before challenge enhances skin delayed type hypersensitivity
             responses to keyhole limpet hemocyanin (KLH)},
   Journal = {PsychoNeuroImmunology Research Society Abstracts},
   Year = {2002},
   Key = {fds69291}
}

@misc{fds69293,
   Author = {Neigh-McCandless, G and Bilbo, SD and Hotchkiss, AH and Nelson,
             RJ},
   Title = {Pyruvate supplementation attenuates stress-evoked
             immunosuppression},
   Journal = {Society for Behavioral Neuroendocrinology
             Abstracts},
   Year = {2002},
   Key = {fds69293}
}

@misc{fds69294,
   Author = {Hotchkiss, AK and Prendergast, BJ and Bilbo, SD and Nelson,
             RJ},
   Title = {Reproductive costs of immune system activation in juvenile
             Siberian hamsters},
   Journal = {Society for Behavioral Neuroendocrinology
             Abstracts},
   Year = {2002},
   Key = {fds69294}
}

@misc{fds69295,
   Author = {Bilbo, SD and Dhabhar, FS and Viswanathan, K and Light, A and Nelson,
             RJ},
   Title = {Sex and photoperiodic differences in immune function and
             stress responses in congeneric hamsters},
   Journal = {Society for Neuroscience Abstracts},
   Year = {2002},
   Key = {fds69295}
}

@misc{fds69296,
   Author = {Neigh-McCandless, G and Bilbo, SD and Hotchkiss, AH and Nelson,
             RJ},
   Title = {Pyruvate supplementation ameliorates the effects of chronic
             stress on immune and endocrine systems},
   Journal = {Society for Neuroscience Abstracts},
   Year = {2002},
   Key = {fds69296}
}

@misc{fds69297,
   Author = {Prendergast, BJ and Hotchkiss, AK and Bilbo, SD and Nelson,
             RJ},
   Title = {Circadian and photoperiodic control of immune function in
             juvenile Siberian hamsters},
   Journal = {Society for Neuroscience Abstracts},
   Year = {2002},
   Key = {fds69297}
}

@misc{fds69298,
   Author = {Bilbo, SD and Dhabhar, FS and Yellon, SM and Nelson
             RJ},
   Title = {Photoperiodic and stress-induced changes in blood and
             splenic leukocyte distributions in Siberian
             hamsters},
   Journal = {Society for Neuroscience Abstracts},
   Year = {2001},
   Key = {fds69298}
}

@misc{fds69299,
   Author = {Bilbo, SD and Nelson, RJ},
   Title = {Photoperiod affects immune function and sickness behavior in
             Siberian hamsters},
   Journal = {Society for Research on Biological Rhythms
             Abstracts},
   Year = {2000},
   Key = {fds69299}
}

@misc{fds69300,
   Author = {Drazen, DL and Bilbo, SD and Nelson, RJ},
   Title = {In vitro melatonin enhancement of splenocyte proliferation
             appears to be mediated directly by melatonin receptor
             subtype 1B},
   Journal = {Society for Behavioral Neuroendocrinology
             Abstracts},
   Year = {2000},
   Key = {fds69300}
}

@misc{fds69301,
   Author = {Bilbo, SD and Drazen, DL and Nelson, RJ},
   Title = {Sickness behavior and energy balance vary as a function of
             photoperiod in Siberian hamsters},
   Journal = {Society for Neuroscience Abstracts},
   Year = {2000},
   Key = {fds69301}
}

@misc{fds69302,
   Author = {Bilbo, SD and Drazen, DL and Bilu, D and Nelson,
             RJ},
   Title = {Luzindole attenuates the in vitro melatonin enhancement of
             cell-mediated immunity in C57BL/6J house
             mice},
   Journal = {Society for Neuroscience Abstracts},
   Year = {1999},
   Key = {fds69302}
}

@misc{fds69303,
   Author = {Bilbo, SD and Klein, SL and DeVries, AC and Nelson,
             RJ},
   Title = {Lipopolysaccharide elicits sexually dimorphic partner
             preference behaviors in monogamous prairie
             voles},
   Journal = {Society for Behavioral Neuroendocrinology
             Abstracts},
   Year = {1999},
   Key = {fds69303}
}

@misc{fds69304,
   Author = {Bilbo, SD and Day, LB and Wilczynski, W},
   Title = {An anticholinergic disrupts operant conditioning but not
             spatial memory in frogs},
   Journal = {Society for Neuroethology Abstracts},
   Year = {1998},
   Key = {fds69304}
}


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