Fig. 2

The scheme represents inflammatory mediators in COPD. Cigarette smoke and other risk factors can activate epithelial cells and also recruit macrophages from circulating monocytes to produce various chemotactic factors that attract inflammatory cells to the lung. For instance, CXCL1, CXCL8, MCP-1, LTB-4, ENA-18, and IL-8 attract neutrophils and monocytes through on CXC-chemokine receptor (CXCR) 2, monocytes also can differentiate to alveolar macrophages in the lung (red arrow). CXCL 9, 10, and 11 can attract CD+8 T cells. IL-23 derived from alveolar macrophages can also trigger th17 entrance to the lung. Recruited macrophages also secrete MMPs (2, 9, 12), elastase, cathepsin K, L, S which are involving in lung fibrosis and emphysema (More detail in Fig. 3). On the other hand, activated lung epithelial cells can secrete TGF-β which leads to fibrosis, and also TNF-α, IL-6, IL-8, and GM-CSF (GM-CSF can increase proliferation of alveolar macrophages (green arrow)). CXCL: CXC-chemokine ligand, IL: interleukin, MCP-1: monocyte chemoattractant protein 1, LTB-4: leukotriene B4, ENA-78: epithelial neutrophil activating peptide, TGF-β: transforming growth factor-beta, GM-CSF: granulocyte–macrophage colony-stimulating factor