Interleukin-17 expression and significance in normal lung function smokers and chronic obstructive pulmonary disease patients

Abstract

To study the effect of interleukin 17 (IL-17) with mechanism of pulmonary inflammatory in smokers with normal lung function and chronic obstructive pulmonary disease (COPD) patients. The peripheral lung cancer patients in need of a surgical therapy were divided into normal lung function and non-smoking group (NS group, n = 10), normal lung function and smoking group (S group, n = 13) and smoking with stable COPD group (COPD group, n = 10). The fresh normal lung tissue was harvested from the surgical specimens with a margin of 5 cm away from resection foci. Then the lung tissue levels of IL-17 were detected with enzyme-linked immunosorbent assay. The average alveolar area, the total small airway pathology score and the pulmonary muscular artery (MA) wall thickness were measured by HE and Victoria blue-Van Gieson's stains. The IL-17+ cells and CD4+, CD8+ lymphocytes in alveolar walls, small airways and lung MA were analyzed by immunohistochemistry. The investigators also explored the relationships between IL-17 level, pathological morphology of pulmonary parenchyma, small airway, pulmonary artery reconstruction and pulmonary functions. The IL-17 levels in lung tissue of NS, S and COPD groups were 6.1 (3.7 - 12.4), 9.7 (3.5 - 69.7) and 22.7 (7.0 - 114.4) pg/mg respectively. The S and COPD groups were significantly higher than the NS group (P < 0.05, P < 0.01). The S group was significantly higher than the NS group (P < 0.05). The average alveolar area were (50 708 +/- 14 125), (106 517 +/- 13 851) and (152 344 +/- 43 783) microm(2), the total small airway pathology score (49 +/- 10), (101 +/- 34) and (163 +/- 36), and the MA wall thickness (119 +/- 11), (139 +/- 25) and (172 +/- 28) microm respectively. The S and COPD groups were significantly higher than the NS group (P < 0.05, P < 0.01). And the COPD group was significantly higher than the S group (P < 0.05, P < 0.01). IL-17 was predominantly expressed in lung infiltration of inflammatory cells. IL-17 of alveolar walls, small airway wall and MA wall in the S and COPD groups were significantly higher than the NS group. And the COPD group was significantly higher than NS group (P < 0.05). IL-17+ cells were positively correlated with the average alveolar area in pulmonary parenchyma (r = 0.561, P < 0.01), the pulmonary artery wall thickness in MA (r = 0.682, P < 0.01) and the pathological score in small airways (r = 0.425, P < 0.05). IL-17+ cells of pulmonary parenchyma, small airways and MA were positively correlated with CD4+ and CD8+ lymphocytes in lung (P < 0.05, P < 0.01). The levels of IL-17 in lung homogenate tissue showed a negative correlation with the FEV(1) percentage of predicted value (r = -0.471, P < 0.01). IL-17 is up-regulated in lung tissues of normal lung function smokers and COPD patients. And it has a close correlation with CD4+ and CD8+ lymphocytes in lung, lung parenchyma destruction, pulmonary inflammation, pulmonary artery reconstruction and airflow limitation. All of these suggest that IL-17 plays an important pro-inflammatory role in COPD.