There are increased numbers of activated T lymphocytes in the bronchialmucosa of stable chronic obstructive pulmonary disease (COPD) patients. Thelper type 17 (Th17) cells release interleukin (IL)-17 as their effector cytokineunder the control of IL-22 and IL-23. Furthermore, Th17 numbers areincreased in some chronic inflammatory conditions.To investigate the expressionof interleukin (IL)-17A, IL-17F, IL-21, IL-22 and IL-23 and of retinoicorphan receptor RORC2, a marker of Th17 cells, in bronchial biopsies frompatients with stable COPD of different severity compared with age-matchedcontrol subjects. The expression of IL-17A, IL-17F, IL-21, IL-22, IL-23 andRORC2 was measured in the bronchial mucosa using immunohistochemistryand/or quantitative polymerase chain reaction. The number of IL-22+ andIL-23+ immunoreactive cells is increased in the bronchial epithelium of stableCOPD compared with control groups. In addition, the number of IL-17A+ andIL-22+ immunoreactive cells is increased in the bronchial submucosa of stableCOPD compared with control non-smokers. In all smokers, with and withoutdisease, and in patients with COPD alone, the number of IL-22+ cells correlatedsignificantly with the number of both CD4+ and CD8+ cells in the bronchialmucosa. RORC2 mRNA expression in the bronchial mucosa was notsignificantly different between smokers with normal lung function andCOPD. Further, we report that endothelial cells express high levels of IL-17Aand IL-22. Increased expression of the Th17-related cytokines IL-17A, IL-22and IL-23 in COPD patients may reflect their involvement, and that of specificIL-17-producing cells, in driving the chronic inflammation seen in COPD.
|Numero di pagine||8|
|Rivista||Clinical and Experimental Immunology|
|Stato di pubblicazione||Published - 2009|