Pneumologie 2017; 71(S 01): S1-S125
DOI: 10.1055/s-0037-1598419
Freie Vorträge – Sektion Zellbiologie
Klinische und experimentelle Grundlagenforschung – Robert Bals/Homburg (Saar), Michael Wegmann/Borstel
Georg Thieme Verlag KG Stuttgart · New York

IL-17A-mediated expression of epithelial IL-17C promotes inflammation during acute Pseudomonas aeruginosa pneumonia

L Wolf
1  Department of Internal Medicine V, Universität des Saarlandes, Homburg (Saar)
,
S Sapich
2  Department of Drug Delivery, Helmholtz Institute for Pharmaceutical Research Saarland, Saarbrücken
,
A Honecker
1  Department of Internal Medicine V, Universität des Saarlandes, Homburg (Saar)
,
M Bischoff
3  Institute of Medical Microbiology and Hygiene, Saarland University Hospital, Homburg (Saar)
,
N Schneider Daum
2  Department of Drug Delivery, Helmholtz Institute for Pharmaceutical Research Saarland, Saarbrücken
,
CM Lehr
4  Helmholtz Institute for Pharmaceutical Research Saarland (Hips), Helmholtz Center for Infection Research (Hzi)
,
F Seiler
1  Department of Internal Medicine V, Universität des Saarlandes, Homburg (Saar)
,
R Bals
1  Department of Internal Medicine V, Universität des Saarlandes, Homburg (Saar)
,
C Beisswenger
1  Department of Internal Medicine V, Universität des Saarlandes, Homburg (Saar)
› Author Affiliations
Further Information

Publication History

Publication Date:
23 February 2017 (online)

 

Lung epithelial cells are suggested to promote pathogen-induced pulmonary inflammation by the release of chemokines, resulting in enhanced recruitment of circulating leukocytes. Recent studies have shown that the interleukin-17C (IL-17C) regulates innate immune functions of epithelial cells in an autocrine manner. The aim of this study was to investigate the contribution of IL-17C to pulmonary inflammation in a mouse model of acute Pseudomonas aeruginosa pneumonia. Infection with P. aeruginosa resulted in an increased expression of IL-17C in lung tissue of wildtype mice. Numbers of neutrophils and the expression of the neutrophil-recruiting chemokines keratinocyte-derived chemokine (KC) and macrophage inflammatory protein 2 (MIP-2) were significantly decreased in lungs of IL-17C-deficient (IL-17C-/-) mice infected with P. aeruginosa at 24 hours. Systemic concentrations of interleukin-6 (IL-6) were significantly decreased in infected IL-17C-/- mice at 24 hours and the survival of IL-17C-/- mice was significantly increased at 48 hours. The expression of IL-17C was reduced in infected mice deficient for interleukin-17A (IL-17A), whereas pulmonary concentrations of IL-17A were not affected by the deficiency for IL-17C. Stimulation of primary alveolar epithelial cells with IL-17A resulted in a significantly increased expression of IL-17C in vitro. Our data suggest that IL-17A-mediated expression of epithelial IL-17C amplifies the release of chemokines by epithelial cells and thereby contributes to the recruitment of neutrophils and systemic inflammation during acute P. aeruginosa pneumonia.