Abstract
Objective To study the role of interleukin-17 (IL-17) in the airway inflammation and remodeling of rats with chronic obstructive pulmonary disease (COPD). Methods Rat models of COPD were replicated by passive smoking for 80 days. Total cell counts and neutrophil counts in bronchoalveolar lavage fluid (BALF) were examined. The thickness of the airway wall and the smooth muscle layer of the small airway were measured by means of image analyzer. The expression of IL-17 in rat lung tissue was detected by immunohistochemistry. The concentrations of IL-17 in lung tissues and tumor necrosis factorα(TNF-α) in BALF and serum were measured with enzyme-linked immunosorbent assay. Results Rat models of COPD were replicated successfully by passive smoking. IL-17 was mainly expressed in airway epithelial cells of COPD rats. The concentrations of IL-17 in lung tissue were significantly higher in the COPD group than in the normal group( P <0. 01). In the COPD group,IL-17 concentration of lung tissue was positively correlated with the neutrophil counts and TNF-α level in BALF( r =0. 65, P <0. 05. r =0. 76, P <0. 01), it also tended to be positively correlated with the thickness of the airway wall and the smooth muscle layer of the small airwayC r =0. 89, P <0. 01. r =0. 80, P <0. 01 ). Conclusions IL-17 probably recruits neutrophils into airways by enhancing the expression of TNF-α,and it may play a role in the airway inflammation and remodeling of COPD. Key words: Chronic obstructive pulmonary disease; Interleukin-17; Tumor necrosis factor alpha; Airway remodeling
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