<i>Il22</i><sup>-/-</sup> mice had improved lung function in terms of airway resistance, total lung capacity, inspiratory capacity, forced vital capacity and compliance.These data highlight important roles for IL-22 and its receptors in human COPD and CS-induced experimental COPD.
This study shows for the first time that a defect in IL-22 is involved in the acute exacerbation induced by NTHi infection during experimental COPD and opens the way to innovative therapeutic strategies.
In this review, we describe current knowledge on the involvement of IL-17 and IL-22 in COPD pathophysiology at steady state and during exacerbations, and discuss implications for COPD management and future therapeutic approaches.
Chronic diseases such as asthma and chronic obstructive pulmonary disease have been associated with IL-17 and IL-22 responses directed against innocuous antigens.
To characterize the frequency of CD4(+)IL-17(+) cells in the lung alveolar walls, small airways and muscular pulmonary arteries of nonsmokers, smokers with normal lung function and COPD patients, CD4(+)IL-17(+) cell number was assessed using double immunofluorescence staining, and IL-17 and IL-21 expression were measured using real-time quantitative PCR in the peripheral lung tissues of 10 nonsmokers, 10 smokers with normal lung function and 10 smokers with stable COPD.
In addition, the number of IL-17A(+) and IL-22(+) immunoreactive cells is increased in the bronchial submucosa of stable COPD compared with control non-smokers.