Effects of diesel exhaust particles on apoptosis related to lung inflammation

Abstract

We have previously reported that components of diesel exhaust particles (DEP) enhance acute lung injury induced by lipopolysaccharide (LPS). However, the underlying mechanisms for the enhancement are not completely explored. This study examined the impacts of DEP components on apoptosis in the lung parenchyma in the presence or absence of LPS. ICR mice were divided into 6 experimental groups that intratracheally received vehicle, LPS (2.5 mg/kg), organic chemicals in DEP (DEP-OC) extracted with dicloromethane (4 mg/kg), residual carbonaceous nuclei of DEP (washed DEP: 4 mg/kg), DEP-OC +LPS, or washed DEP+LPS. Detection of apoptosis in the lung was evaluated 24 hours after the intratracheal administration. As compared to vehicle, DEP components did not induce a significant increase in the number of apoptotic cells in the lung. LPS significantly increased the number as compared with vehicle. The number of apoptotic cells was significantly greater in the DEP component groups than in the LPS group. These findings suggest that DEP enhance apoptosis in the lung in the presence of LPS. Enhanced apoptotic effects of DEP components, thus, may play a role in the pathogenesis of abrogated lung injury by the components related to bacterial endotoxin.