INFLAMMATORY CELLS AND THEIR MEDIATORS IN COPD PATHOGENESIS

INFLAMMATORY CELLS AND THEIR MEDIATORS IN COPD PATHOGENESIS Chronic Obstructive Pulmonary Disease (COPD) is considered to be a progressive disease characterized by chronic inflammation and irreversible airflow obstruction, mainly caused by tobacco smoking. Based on World Health Organization data, COPD will be the fourth cause of mortality in 2020, after vascular, cardiac and cerebral diseases and cancer. To date no therapy retards or suppresses progression of COPD. The chronic inflammatory process caused by tobacco smoking promotes structural changes predominantly in the small airways (less than 2mm). Macrophages, neutrophils and T cells are thought to be important key players, as well as structural cells like fibroblasts, epithelial and smooth muscle cells. The interaction between macrophages and lymphocytes, especially CD8+, has been implicated in the pathogenesis of COPD. Chemokines such as CXCL9/MIG, CXCL10/IP-10, CXCL11/I-TAC and CCL5/RANTES have been described as possibly responsible for recruitment of T cells and blood monocytes increasing the number of macrophages and CD8+ T cells in the lung of COPD patients. The study of the influx of mononuclear cells to the lung is very important not only to promote a better understanding of the COPD physiopathology but also to help identify new targets for treatment. Based on this new evidence, the study of several mediator antagonists that can block the recruitment of inflammatory cells to the lung have been tested in COPD. [Rev Assoc Med Bras 2009; 55(3): 347-54]