TY - JOUR T1 - IL-17C is expressed in respiratory epithelial cells under inflammatory conditions JF - European Respiratory Journal JO - Eur Respir J VL - 40 IS - Suppl 56 SP - 4734 AU - Philipp Pfeifer AU - Jan Hellberg AU - Philipp Lepper AU - Frank Langer AU - Robert Bals AU - Christoph Beisswenger Y1 - 2012/09/01 UR - http://erj.ersjournals.com/content/40/Suppl_56/4734.abstract N2 - 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. ER -