RT Journal Article
SR Electronic
T1 Differential function of IL-17A in cigarette smoke induced lung damage
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP P1850
VO 44
IS Suppl 58
A1 Meike Voss
A1 Bodo Wonnenber
A1 Andreas Kamyschnikow
A1 Christian Herr
A1 Michael Wegmann
A1 Michael Menger
A1 Robert Bals
A1 Christoph Beisswenger
YR 2014
UL http://erj.ersjournals.com/content/44/Suppl_58/P1850.abstract
AB Smoking is the main risk factor for the chronic obstructive pulmonary disease (COPD). A recent study demonstrated by quantitative microcomputed tomography (µCT) that IL-17A-deficient mice exposed to cigarette smoke are protected from increases in lung volume and decreased lung density. This suggests that Th-17/IL-17-dependent immune mechanisms mediate smoke-induced lung damage, such as the development of emphysema. Here, we demonstrate a more complex role of IL-17A in the development of lung damage in mice chronically exposed to smoke. Physiologically relevant pulmonary function showed that IL-17A deficient mice were per se not protected from smoke-induced emphysematous disease. Respiratory compliance was increased in IL-17-deficient mice after smoke exposure, even though IL-17-deficient mice were partially protected from smoke-induced changes in the total lung capacity and hysteresis. Histology and morphometry showed that smoke-exposure results in loss of lung structure in IL-17-deficient mice. These results suggest that, in the present disease model, IL-17A rather has a protective than a deleterious role in smoke-induced loss of lung function.