Pneumologie 2013; 67 - P89
DOI: 10.1055/s-0033-1334617

IL-17C is a mediator of respiratory epithelial innate immune response

P Pfeifer 1, M Voss 1, B Wonnenberg 1, M Bischoff 2, F Langer 3, R Bals 1, C Beisswenger 1
  • 1Saarland University, Department of Internal Medicine V – Pneumology, Allergology and Respiratory Critical Care Medicine, Homburg (Saar)
  • 2Saarland University, Institute of Medical Microbiology and Hygiene, Homburg (Saar)
  • 3Saarland University, Department of Thoracic and Cardiovascular Surgery, Homburg (Saar)

Aims: 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: We show that common bacterial pathogens such as Pseudomonas aeruginosa and Haemophilus influenzae and ligands of Toll-like receptors 3 and 5 (flagellin, polyI:C) induced the expression and release of IL-17C in cultured human bronchial epithelial cells (HBECs). The expression of IL-17A, B, D, or E was not induced by bacterial stimuli in HBECs. IL-17C enhanced inflammatory responses of respiratory epithelial cells infected with P. aeruginosa. Further, we demonstrate that cigarette smoke suppressed the expression of IL-17C in HBECs in response to bacterial infection and in vivo in the upper airways of mice colonized with H. influenzae. IL-17C could also 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.