The Changes And Significance Of Interleukin-16 And CXCR3 In Pulmonary Artery Of Smokers And Patients With Chronic Obstructive Pulmonary Disease

Objective To study the pathological characteristics of interleukin-16 and CXCR3 in pulmonary artery of smokers with normal lung function and smokers with chronic obstructive pulmonary disease (COPD).Methods 33 patients who were underwent lung resection for localized pulmonary lesions, were devided into three groups: group NS (Nonsmokers with normal lung function, n=10); group S (Smokers with normal lung function, n=13); group COPD (Smokers with stable COPD, n=10). The clinical data including blood gas analysis, pulmonary function, body-mass index(BMI), smoking index, BODE index, six-minute-walk distance (6MWD), MRC, were recorded in all subjects before the operation. We applied technique of hematoxylin-eosin staining to observe pathomorphological changes of the pulmonary arteries. The concentration of IL-16 in lung tissues was measured by enzyme-linked immunsorbent assay (ELISA). T-lymphocytes(CD3), CD4+T-lymphocytes, CD8+T-lymphocytes, IL-16, CXCR3 were identified by immunohistochemistry in muscularized arteries. The correlation test was used to assess relationships between IL-16 and CXCR3 in muscularized arteries of group S and group COPD and some clinical data. Results (1)Group COPD showed the highest concentration of IL-16 in lung tissue (P<0.01) . The concentration of IL-16 in group S was higher than group NS (P<0.05). (2) Both in group S and in group COPD, range and degree of the CXCR3 and IL-16 positive cells expressed in MA was higher than that in group NS (P<0.01). (3) The intensity of IL-16 infiltrating the muscularized arteries in group S showed a positive correlation with CD8+T-lymphocytes,CXCR3,smoking index(r=0.675,0.642,0.619,P<0.05)。We also found the intensity of CXCR3 infiltrating the muscularized arteries in group S showed a positive correlation with CD8+T-lymphocytes,smoking index (r=0.583,0.602,P<0.05)。The intensity of IL-16 infiltrating the muscularized arteries in group COPD showed a positive correlation with T-lymphocytes,CD8+T-lymphocytes,CXCR3 (r=0.639,0.803,0.696. P<0.05 or P <0.01), BODE index (r=0.704. P<0.05). The content of IL-16 in the muscularized arteries in group COPD was inversely related to FEV1% Pred. and 6MWD (r=-0.803,-0.787. P<0.01). We also found the intensity of CXCR3 infiltrating the muscularized arteries in group COPD showed a positive correlation with T-lymphocytes,CD8+T-lymphocytes (r=0.650,0.767. P<0.05), BODE index (r=0.767.P<0.05). The content of CXCR3 in the muscularized arteries in group COPD was inversely related to FEV1% Pred. and 6MWD (r=-0.778,-0.774. P <0.01).Conclusions (1) Both in group S and in group COPD, the expressions of IL-16 and CXCR3 were observed mainly in inflammatory cells and were correlated with CD8+T-lymphocytes infiltrating the muscularized arteries. These findings suggest that IL-16 might recruit CD8+T-lymphocytes into muscularized arteries by up regulating the expression of CXCR3, which may be involved in the pulmonary arterial inflammation. (2) The intensities of IL-16 and CXCR3 were correlated with the index of clinical and pulmonary function, suggesting that pulmonary arterial inflammation might be one of key factors in the progression of COPD.