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. Author manuscript; available in PMC: 2010 Aug 1.
Published in final edited form as: Curr Opin Pharmacol. 2009 Jul 15;9(4):375–383. doi: 10.1016/j.coph.2009.06.009

Figure 1. Cells and mediators involved in the pathogenesis of COPD and lung cancer.

Figure 1

Exposure to cigarette smoke or other pollutants/toxicants induces the release of chemokines from macrophages and epithelial cells which further attract other inflammatory and immune cells including neutrophils, T-cells, and B-cells into the lungs. As a result of influx of these inflammatory cells, proteases, perforin, and granzyme are released leading to alveolar wall destruction and mucus hypersecretion. Furthermore, activated B-cells produce autoantibodies against elastin, epithelium, and endothelium leading to autoimmune impairment in lungs. Epithelial cells and macrophages also release TGF-β leading to small airway remodeling through activation/differentiation of fibroblasts to myofibroblasts. Cigarette smoke is shown to induce the release of VEGF from epithelial cells leading to angiogenesis which plays an important role in progression, invasion, and metastasis of lung cancer. Interestingly, VEGF receptor 2 in endothelial cells is downregulated by cigarette smoke leading to endothelial dysfunction which occurs in emphysema.