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| Publications [#119289] of Bernard M Fischer
Papers Published
- TM Krunkosky, BM Fischer, NJ Akley, KB Adler, Tumor necrosis factor alpha (TNF alpha)-induced ICAM-1 surface expression in airway epithelial cells in vitro: possible signal transduction mechanisms.,
Annals of the New York Academy of Sciences, vol. 796
(October, 1996),
pp. 30-7, ISSN 0077-8923
(last updated on 2013/05/16)
Abstract:
Within the past several years research on the interaction of cytokines and adhesion molecules with airway epithelium in diseases has allowed us to develop a better understanding of the disease process. The cytokine, TNF alpha and the adhesion molecule ICAM-1 are important mediators in the pathogenesis of airway diseases such as asthma, chronic bronchitis, and adult respiratory distress syndrome. Effects of TNF alpha on ICAM-1 surface expression was investigated in both primary cultures of normal human bronchial epithelial (NHBE) cells and immortalized human bronchial epithelial cell line BEAS-2B. TNF alpha (0.015-150 ng/mL) significantly enhanced ICAM-1 surface expression (measured by flow cytometry) in a dose and time-dependent manner, with peak expression seen at 24 hours. This response was negated by heat inactivation of the TNF alpha prior to incubation. TNF alpha-induced ICAM-1 expression also was inhibited by pre- and coincubation of TNF alpha with 3 micrograms/mL soluble TNF-R1 or by the PKC inhibitor, Calphostin C (0.1 and 0.5 microM). The ROI scavengers, dimethylthiourea (4 mM), and dimethyl sulfoxide (0.001%), enhanced TNF alpha-induced ICAM-1 expression. Collectively, these results indicate that TNF alpha-induced ICAM-1 surface expression is a specific receptor-mediated response (TNF-R1), which is mediated by mechanisms dependent on PKC and intracellular reactive oxygen species.
Keywords:
Adult • Antigens, CD • Antioxidants • Bronchi • Cell Line • Epithelium • Flow Cytometry • Humans • Intercellular Adhesion Molecule-1 • Protein Kinase C • Receptors, Tumor Necrosis Factor • Receptors, Tumor Necrosis Factor, Type I • Signal Transduction* • Tumor Necrosis Factor-alpha • cytology* • metabolism • metabolism* • pharmacology • pharmacology*
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