Increased expression of CD4+IL-17+ cells in the lung tissue of patients with stable chronic obstructive pulmonary disease (COPD) and smokers

CD4+IL-17+ cells have an important role in controlling immune and inflammatory reactions. The authors of the present study hypothesize that these cells may be involved in the pathogenesis of chronic obstructive pulmonary disease (COPD). 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 the lung alveolar walls, the number of CD4+IL-17+ cells was increased in COPD patients compared with nonsmokers and in normal smokers compared with nonsmokers. In the small airways, the CD4+IL-17+ cell numbers were higher in COPD patients than in normal smokers and nonsmokers. A positive correlation was observed between CD4+IL-17+ cell expression and pathological changes in the lung tissue. In the small airways, the number of CD4+IL-17+ cells was positively correlated with airflow limitations. The IL-17 mRNA levels in lung tissues were increased in COPD patients and normal smokers compared with nonsmokers. Increased CD4+IL-17+ cell number in lung tissue is involved in chronic inflammation of the lungs and parallels lung injury aggravation in COPD patients and in smokers without airway limitations. These findings contribute to a better understanding of CD4+ cell-related pathogenesis in COPD.

► There is an increased number of CD4+IL-17+ cell in the lung tissues of COPD patients.
► The increased CD4+IL-17+ cell was in line with pathological injury of COPD lung.
► The increased CD4+IL-17+ cell was correlated to airway limitation of COPD patients.
► CD4+ cell may participate lung inflammation through IL-17 in COPD pathogenesis.