[Relationships between the expressions of intercellular adhesion molecule-1 and tissue inhibitor of metalloproteinase-1 and matrix metalloproteinase-9 in lung tissues of patients with chronic obstructive pulmonary disease].

To evaluate the correlation between the expressions of intercellular adhesion molecule-1 (ICAM-1) and tissue inhibitor of metalloproteinase-1 (TIMP-1) and matrix metalloproteinase-9 (MMP-9) in lung tissues of patients with COPD. Lung tissues from patients with COPD (COPD group, n = 19) and those without COPD (smokers and nonsmokers with normal lung function, n = 11 and 9, respectively) were obtained from surgical excisions of lung cancer patients. The mRNA expression of ICAM-1, TIMP-1 and MMP-9 was detected using semi-quantitative RT-PCR. The protein expression of ICAM-1, TIMP-1 and MMP-9 was detected by using immunohistochemistry method. There were significant differences in FEV1% and FEV1/FVC% among smokers without COPD, nonsmokers without COPD and COPD patients. MMP-9 was highly expressed in alveolar epithelial cells, bronchial epithelial cells, vascular smooth muscle cells, alveolar macrophages, and interstitial cells in the COPD group, compared with smokers without COPD group and nonsmokers without COPD group (54.0 +/- 15.0), (1.2 +/- 0.7) and (1.4 +/- 0.8). Low level expression of TIMP-1 was detected in alveolar macrophages, alveolar epithelial cells and vascular smooth muscle cells in the COPD group, but no expression in smokers and nonsmokers without COPD. High level expression of ICAM-1 was detected in alveolar epithelial cells, and the expression was higher in the COPD group (52.1 +/- 13.4), (2.1 +/- 1.1) and (4.5 +/- 2.4). The mRNA level of MMP-9 showed significant difference among patients with COPD, smokers without COPD and nonsmokers without COPD (0.71 +/- 0.16), (0.20 +/- 0.08) and (0.17 +/- 0.05). The mRNA level of TIMP-1 was also significantly different among patients with COPD, smokers without COPD and nonsmokers without COPD (0.47 +/- 0.10), (0.26 +/- 0.08) and (0.20 +/- 0.06). ICAM expression was also significantly higher in patients with COPD as compared with smokers without COPD and nonsmokers without COPD (0.62 +/- 0.15), (0.44 +/- 0.12) and (0.37 +/- 0.11). Both the mRNA and the protein levels of MMP-9 were inversely correlated with FEV1 % and FEV1/FVC% (r= -0.759, -0.756, -0.772, -0.725, respectively, P <0.01). TIMP-1 mRNA level was inversely correlated with FEV1% and FEV1/FVC% (r = -0.675, -0.623, respectively P <0.01). Negative correlations were also noted between ICAM-1 expressions (both mRNA and protein) and FEV1% or FEV1/FVC% (r = -0.580, -0.531, -0.739, -0.756, respectively P <0.01). Interestingly, the mRNA expression of TIMP-1, MMP-9 and ICAM-1 was positively correlated (r = 0.576, 0.524, P < 0.01), while the protein levels of MMP-9 and ICAM-1 were positively correlated (r = 0.964, P <0.01). There was a significant correlation between over-expression of ICAM-1 and TIMP-land MMP-9 in lung tissues from COPD patients. Over-expressions of ICAM-1 in the lung may result in accumulation of inflammatory cells releasing certain inflammatory factors that could destroy the normal lung structure. In addition, highly expressed TIMP-1 and MMP-9 in lung tissues may also contribute to the destruction and reconstitution of the bronchial or/and alveolar wall, which is likely to play a major role in airway obstruction.

Kong YJ ，Sun WX ，Zhang YM ，Shi YZ ... -  《-》

Pathogenesis of cigarette smoke-induced chronic obstructive pulmonary disease and therapeutic effects of glucocorticoids and N-acetylcysteine in rats.

Xu L ，Cai BQ ，Zhu YJ 《CHINESE MEDICAL JOURNAL》

[Metalloproteinase-9/tissue inhibitor of metalloproteinase-1 in induced sputum in patients with asthma and chronic obstructive pulmonary disease and their relationship to airway inflammation and airflow limitation].

Xin XF ，Zhao M ，Li ZL ，Song Y ，Shi Y ... -  《-》

[The role of matrix metalloproteinases-9 and tissue inhibitor of metalloproteinaes-1 in chronic obstructive pulmonary disease].

Xu XM ，Sun TY ，Lin JB ，Zhang HS ... -  《-》

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

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.

Zhang JQ ，Lao QF ，Chu SY ，Bai J ，Zhong XN ... -  《-》