Plasminogen activator inhibitor-1 promotes inflammatory process induced by cigarette smoke extraction or lipopolysaccharides in alveolar epithelial cells.

Plasminogen activator inhibitor-1 (PAI-1) plays a role in regulating levels of some cytokines and cell migration in addition to its classic role in inhibiting fibrinolysis. PAI-1 levels in induced-sputum of chronic obstructive pulmonary disease (COPD) patients were elevated significantly and correlated negatively with pulmonary function. To study the role of PAI-1 in inflammatory process in COPD, the authors transfected alveolar epithelial cells (AECs) with siRNA-targeted PAI-1 and stimulated the cells by cigarette smoke extraction (CSE) or lipopolysaccharides (LPS). The expression of inflammatory factors, interleukin-8 (IL-8) and leukotriene B4 (LTB4), and the monocyte migration were detected. The exposure to CSE or LPS induced the expression of PAI-1, IL-8, and LTB4 in AECs and monocyte migration to AECs. However, they were attenuated after transfection with siRNA-targeted PAI-1. In conclusion, PAI-1 stimulates inflammation induced by CSE or LPS in AECs through up-regulation of inflammatory factors and promoting inflammatory cell migration. PAI-1 may play a proinflammatory role in the pathogenesis of COPD.