OBJECTIVE: To study the pathological characteristics of interleukin-16 (IL-16) and CXC chemokine receptor 3(CXCR3) in pulmonary artery of smokers with normal lung function and smokers with chronic obstructive pulmonary disease (COPD). METHODS: We examined surgical specimens from three groups of subjects undergoing lung resection for localized pulmonary lesions: 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 datas including blood gas analysis, pulmonary function, BMI, smoking index, BODE index, six-minute-walk distance (6MWD), Medical Research Council dyspnea scale (MRC), St. George Respiratory Questionnaire (SGRQ) 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 were measured by ELISA. Muscularized arteries were examined with immunohistochemical methods to identify T-lymphocytes (CD(3)), CD(4) T-lymphocytes, CD(8) T-lymphocytes, IL-16, CXCR3. The correlation of IL-16 and CXCR3 in muscularized arteries in smokers with stable COPD were analysed. RESULTS: (1) The 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 group COPD, the percentage of the muscularized arteries that contained CXCR3 and IL-16 were increased as compared with group NS (P < 0.01). Moreover there were statistical significance have been observed between group COPD and group S (P < 0.01). (3) The intensity of IL-16 infiltrating the muscularized arteries in group COPD showed a positive correlation with CD(3)(+)T-lymphocytes, CD(8)(+)T-lymphocytes, CXCR3 (r = 0.639, 0.803, 0.696; P < 0.05 or P < 0.01), smoking index, BODE index (r = 0.737, 0.704; P < 0.05). There was inverse relationship between the content of IL-16 in the muscularized arteries in group COPD and forced expiratory volume in one second% predicted (FEV(1)% 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 CD(3)(+) T-lymphocytes, CD(8)(+)T-lymphocytes (r = 0.650, 0.767; P < 0.05), smoking index, BODE index (r = 0.650, 0.767; P < 0.05). There was inverse relationship between the content of CXCR3 in the muscularized arteries in group COPD and FEV(1)% Pred and 6MWD (r = -0.778, -0.774; P < 0.01). CONCLUSIONS: (1) Both in group S and group COPD, IL-16 and CXCR3 were mainly expressed in lymphocytes which were correlated with CD(8)(+)T-lymphocytes infiltrating the muscularized arteries. There were some suggestion that IL-16 probably recruited CD(8)(+)T-lymphocytes into muscularized arteries by enhancing the expression of CXCR3. (2) The intensity of IL-16 and CXCR3 were correlated with the index of clinical and pulmonary function that suggested pulmonary arterial inflammation might be one of the key factors associated with the progression of COPD, and inhibiting the pulmonary artery inflammation played an important role in prevention and cure of COPD.