Cigarette smoke-elastase interactions in the pathogenesis of emphysema

The results support the concept that prior or coexistent cigarette smoke exposure might modify protease-induced lung injury from some other cause to result in emphysema. Possible mechanisms for this effect include: oxidative inactivation of alpha₁-antiproteinase directly by cigarette smoke or indirectly via smoke-induced recruitment of lung phagocytes; increased protease levels from smoke-recruited phagocytes; cigarette smoke-induced defects in lung repair; or other smoke-induced alterations in lung structure or function which enhance susceptibility to protease damage.