Study on the expression of Toll-like receptor 4 and matrix metalloproteinase-9 in patients with chronic obstructive pulmonary disease and their clinical significance

Y. Zhang, H.-J. Ni, H.-S. Zhou

Department of Respiratory Medicine, The Affiliated Hospital of Panzhihua University, Panzhihua, Sichuan Province, China. rw5z86@163.com

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• Neurology

OBJECTIVE: To investigate the expression of Toll-like receptor 4 (TLR4) and matrix metalloproteinase-9 (MMP-9) in patients with chronic obstructive pulmonary disease (COPD) and their clinical significance.

PATIENTS AND METHODS: Paracancerous tissues from 48 patients with lung squamous cell carcinoma harvested during pulmonary lobectomy were studied. Twenty-four cases of COPD were chosen as the observation group and 24 cases of non-COPD as the control group. The degree of lung inflammation was observed; the ratio of the thickness of the wall to the external diameter of the pulmonary arterioles (WT%), and the ratio of the area of the wall to that of the pulmonary arterioles (WA%) were calculated. Immunohistochemistry was used to evaluate the expression of TLR4, MMP-9, and proliferating cell nuclear antigen (PCNA) in vascular smooth muscle cells, and the expressions were correlated with lung revascularization.

RESULTS: (1) Compared with the non-COPD group, the degree of inflammatory cell infiltration, WA%, and WT% of the COPD group were significantly increased (p<0.05). Additionally, the expression of TLR4, MMP-9, and PCNA in vascular smooth muscle cells was significantly increased (p<0.05). (2) Correlative analysis revealed that the expression of TLR4 and MMP-9 had significant positive correlation with the degree of inflammatory cell infiltration, WA%, WT%, and PCNA expression (p<0.05). Multivariate regression analysis showed that, compared with the smoking index and inflammation score, TLR4 and MMP-9 expression were the strongest factors affecting the parameters of lung revascularization (WA% and WT%) (p<0.05).

CONCLUSIONS: High expression of MMP-9 and TLR4 in patients with COPD may promote inflammatory cell infiltration, induce proliferation of smooth muscle cells, degrade extracellular matrix, and play an important role in lung revascularization.

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