Diesel exhaust particles synergistically enhance lung injury and oxidative stress induced by bacterial endotoxin

Epidemiologic studies have demonstrated acute and serious adverse effects of particulate air pollution on respiratory health, especially in people who are susceptible to bacterial infection. The underlying mechanism remains to be elucidated. Diesel exhaust particles (DEP) derived from diesel engine-powered automobiles are major constituents of the atmospheric particular matter in metropolitan areas. DEP reportedly enhance airway inflammation and lung injury. Bacterial endotoxin in a purified form known as lipopolysaccharide is also implicated as an environmental factor that exacerbates lung diseases. In this article, we review the synergistic enhancing effects of DEP and bacterial endotoxin on airway inflammation and determine the components in DEP responsible for these effects. Oxygen free radicals and proinflammatory cytokines are proposed mediators for DEP-induced airway inflammation. We elucidate the role of oxidative stress and proinflammatory cytokine expression in the enhancement.