Differential function of IL-17A in cigarette smoke induced lung damage

Abstract

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.