Cigarette Smoke-Induced Pulmonary Inflammation and Emphysema Are Attenuated in CCR6-Deficient Mice

摘要: Chronic obstructive pulmonary disease (COPD) is mainly caused by cigarette smoking, and characterized an increase in inflammatory cells the airways tissue. The chemokine receptor CCR6 its ligand MIP-3α/CCL20 may be involved recruitment of these cells. To investigate role pathogenesis COPD, we analyzed responses knockout (KO) wild-type mice upon smoke (CS) exposure. Both subacute chronic exposure to CS induced innate adaptive immune system bronchoalveolar lavage, both KO mice. However, accumulation dendritic cells, neutrophils, T lymphocytes, which express CCR6, was significantly attenuated mice, compared with their littermates. In lung tissue there impaired activated CD8 + granulocytes. Moreover, this response offered a partial protection against emphysema, correlated production MMP-12. Importantly, protein levels MIP-3α/CCL20, only receptor, MCP-1/CCL2 were increased wild-type, but not contrast, deficiency had no effect on development airway wall remodeling These results indicate that interaction MIP-3α contributes CS-induced inflammation emphysema murine model COPD.