[Effect of IL-17 on ICAM-1 expression of human bronchial epithelial cells, NCI-H 292].
Bronchial asthma is characterized as a chronic inflammation of the airway infiltrated by eosinophils, lymphocytes, and neutrophils. ICAM-1 expression on airway epithelium facilitates adhesion between these inflammatory cells and bronchial epithelial cells, and induces the activation of inflammatory cells. ICAM-1 expression was affected by various cytokines, such as IL-17. IL-17 is a novel cytokine released by CD4+ activated memory T cells. In this study, we examined the effect of IL-17 on ICAM-1 expression by RT-PCR and flow cytometry. Human bronchial epithelial cells, NCI-H 292 cells, were stimulated with IL-17 (100 ng/ml) and/or IFN-gamma (100 U/ml). ICAM-1 was expressed constitutively. IL-17 alone did not enhance ICAM-1 expression on NCI-H 292 cells. However, IL-17 synergistically enhanced ICAM-1 expression induced by IFN-gamma. These results suggest that IL-17 has an effect on ICAM-1 expression of bronchial epithelial cells in airway inflammation.
Kawaguchi
M
M
First Department of Internal Medicine, School of Medicine, Showa University.
Kokubu
F
F
Kuga
H
H
Tomita
T
T
Matsukura
S
S
Hoshino
H
H
Imai
T
T
Adachi
M
M
D001980:Bronchi / Q000166:cytology*; D002478:Cells, Cultured; D004357:Drug Synergism; D004847:Epithelial Cells / Q000378:metabolism*; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism*; D007371:Interferon-gamma / Q000494:pharmacology; D020381:Interleukin-17 / Q000494:pharmacology* / Q000502:physiology; D013268:Stimulation, Chemical
D020381:Interleukin-17; D018799:Intercellular Adhesion Molecule-1; D007371:Interferon-gamma