title: IL-17C is a mediator of respiratory epithelial innate immune response.
abstract: The IL-17 family of cytokines consists of at least six members (IL-17A to -F). IL-17 directly activates epithelial cells leading to the expression of inflammatory mediators and antimicrobial factors. Recent studies showed that IL-17C is expressed by epithelial cells. It was the purpose of this study to examine the expression of IL-17 family members in respiratory epithelial cells during bacterial infection. 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. Furthermore, 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. These data show that IL-17C is involved in the innate immune response of respiratory epithelial cells and is suppressed by cigarette smoke.
authors.affiliation: Department of Internal Medicine V-Pneumology, Allergology and Respiratory Critical Care Medicine, Saarland University Medical Center, Homburg/Saar, Germany.
authors.forename: Philipp
authors.initials: P
authors.lastname: Pfeifer
authors.forename: Meike
authors.initials: M
authors.lastname: Voss
authors.forename: Bodo
authors.initials: B
authors.lastname: Wonnenberg
authors.forename: Jan
authors.initials: J
authors.lastname: Hellberg
authors.forename: Frederik
authors.initials: F
authors.lastname: Seiler
authors.forename: Philipp M
authors.initials: PM
authors.lastname: Lepper
authors.forename: Markus
authors.initials: M
authors.lastname: Bischoff
authors.forename: Frank
authors.initials: F
authors.lastname: Langer
authors.forename: Hans-Joachim
authors.initials: HJ
authors.lastname: Schäfers
authors.forename: Michael D
authors.initials: MD
authors.lastname: Menger
authors.forename: Robert
authors.initials: R
authors.lastname: Bals
authors.forename: Christoph
authors.initials: C
authors.lastname: Beisswenger
mesh_terms: D000818:Animals; D001980:Bronchi / Q000276:immunology / Q000473:pathology; D002460:Cell Line; D005786:Gene Expression Regulation / Q000187:drug effects / Q000276:immunology; D006192:Haemophilus Infections / Q000276:immunology* / Q000473:pathology; D006193:Haemophilus influenzae / Q000276:immunology*; D006801:Humans; D007113:Immunity, Innate; D007249:Inflammation / Q000276:immunology / Q000473:pathology; D020381:Interleukin-17 / Q000276:immunology*; D051379:Mice; D011552:Pseudomonas Infections / Q000276:immunology* / Q000473:pathology; D011550:Pseudomonas aeruginosa / Q000276:immunology*; D020545:Respiratory Mucosa / Q000276:immunology* / Q000473:pathology; D012907:Smoking / Q000276:immunology / Q000473:pathology; D014028:Tobacco Smoke Pollution / Q000009:adverse effects
chemical_list: C515930:Il17c protein, mouse; D020381:Interleukin-17; D014028:Tobacco Smoke Pollution