Abstract
The experimental evidences linking PM2.5 exposure to weight status disorder and the associated mechanisms were lacked. Here, we demonstrated exposure of 198.52 μg/m3 PM2.5 (Baoji city, China) for 40 days induced body weight loss of male Balb/C mice, and then increased after 14-day recovery. Correspondingly, gut microbiota dysbiosis, ileum metabolism alterations, and histopathological changes of liver and ileum elucidated the underlying mechanism. The richness and function modules of flora in feces significantly reduced after exposure, and the ratios of Bacteroidetes/Firmicutes reduced from 1.58 to 0.79. At genus level, Lactobacillus and Clostridium increased markedly, while Bacteroides and Parabacteroides decreased at day 40. After recovery, Oscillospira became the dominant genus. Additionally, the key metabolites in the ileum mediated by PM2.5 identified by metabolomics included arachidonic acid, prostaglandin H2, prostaglandin F2α, 5(S)-HPETE, AMP, and deoxyadenosine. Accordingly, conjoint analysis between the gut micorbiota and metabolic profiling revealed suppression of Arachidonic acid metabolism, linoleic acid metabolism, and PPAR signaling pathway and stimulation of ABC transporters might contribute to the liver injury, ileum inflammation, and then weight loss of mice. Our findings suggested PM2.5 affected weight status of mice by meditating intestinal microenvironment, and provided new insight for further diagnosis of the air pollution dependent disease.