RT Journal Article
SR Electronic
T1 IL-17C is expressed in respiratory epithelial cells under inflammatory conditions
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP 4734
VO 40
IS Suppl 56
A1 Philipp Pfeifer
A1 Jan Hellberg
A1 Philipp Lepper
A1 Frank Langer
A1 Robert Bals
A1 Christoph Beisswenger
YR 2012
UL http://erj.ersjournals.com/content/40/Suppl_56/4734.abstract
AB Background: IL-17 is a cytokine that comprises a group of five IL-17 subtypes (IL-17 A to F). IL-17 directly activates epithelial cells leading to the expression of inflammatory mediators and antimicrobial factors. Recent studies showed that IL-17A/F is released by professional immune cells such as CD4+ T cells and macrophages whereas IL-17C is expressed by epithelial cells. It was the purpose of this study to examine the expression of IL-17 in respiratory epithelial cells infected with bacterial pathogens.Methods: Bronchial epithelial cells were exposed to smoke and infected with bacterial pathogens. Mice were exposed to smoke and colonized with H. influenza. Expression and release of IL-17 (A to F) was measured by ELISA and qRT-PCR. IL-17C was detected in human bronchial tissue by immunohistochemistry.Results: Bacterial pathogens such as P. aeruginosa and H. influenzae induced the expression and release of IL-17C in human bronchial epithelial cells (HBECs). The same was true for ligands of Toll-like receptors 3 and 5 (flagellin, polyI:C). The expression of IL-17A/B/D/E was not induced by bacterial stimuli in HBECs. Cigarette smoke suppressed the expression of IL-17C in HBECs in response to bacterial infection in vitro and in the upper airways of mice colonized with H. influenza in vivo. IL-17C could be detected in bronchial tissue of subjects with infection-related lung diseases.Conclusion: These data show that IL-17C is involved in the innate immune response of respiratory epithelial cells. Smoke suppresses IL-17C expression in case of infection.