PM2.5 exposure aggravates acute liver injury by creating an inflammatory microenvironment through Kupffer cell.

This work aimed to investigate the impact of PM2.5 exposure on acute liver injury C57BL/6 mice were used to examine the hepatic histopathological changes in PM2.5-exposed mice, as well as in CCl4-mediated acute liver injury mice after long-term exposure to PM2.5. During in vitro experiments, Kupffer cells were detected for M1 polarization level after treating with PM2.5, and the activation level of NLRP3 inflammasomes were assessed. According to our findings, PM2.5 can induce M1 polarization of Kupffer cells in the liver to create an inflammatory microenvironment. Long-term exposure to PM2.5 can aggravate acute liver injury in mice. Treatment with MCC950, an NLRP3 inhibitor, can inhibit the effect of PM2.5. As demonstrated by in vitro analysis, PM2.5 can promote M1 polarization of Kupffer cells. As suggested by our results, long-term exposure to PM2.5 can create an inflammatory microenvironment to aggravate mouse acute liver injury. The effect is related to NLRP3-mediated M1 polarization in Kupffer cells. • PM2.5 can create an inflammatory microenvironment to aggravate acute liver injury. • The effect is related to NLRP3-mediated M1 polarization in Kupffer cells. • PM2.5 exerts its effects through activating NLRP3. [ABSTRACT FROM AUTHOR]