IL-17C associates with disease severity during acute exacerbation of chronic obstructive disease and promotes neutrophilic lung inflammation

<b>Background:</b> Chronic neutrophilic inflammation contributes to lung destruction in chronic obstructive pulmonary disease (COPD). The pro-inflammatory cytokine IL-17C is expressed by airway epithelial cells and regulates neutrophilic chemotaxis. Here, we examined whether the amount of IL-17C associates with disease severity during acute exacerbation of chronic obstructive pulmonary disease (AECOPD). We further studied the function of IL-17C in a model of inflammation-induced lung damage. <b>Methods:</b> IL-17C was measured in sputum samples obtained during AECOPD. Mice deficient for IL-17C were subjected to a model of nontypeable <i>Haemophilus influenzae</i>- (NTHi) induced COPD-like lung inflammation. <b>Results:</b> Concentrations of IL-17C were significantly increased during advanced COPD (GOLD III/IV) compared to moderate COPD (GOLD I/II). The expression of neutrophilic cytokines and neutrophilia were significantly decreased in mice deficient for IL-17C. <b>Conclusion:</b> IL-17C may contribute to the progression of COPD and be a therapeutic target during AECOPD.