PM2.5 exposure perturbs lung microbiome and its metabolic profile in mice

Abstract

Fine particulate matter (PM2.5) have become a major public health concern because of their adverse effects on health. Lungs are considered the primary organ affected by PM2.5. In order to understand the mechanism underlying PM2.5-induced lung injury, 16S rRNA gene sequencing, and liquid chromatography-mass spectrometry (LC-MS) metabolomics analysis were conducted to investigate the impact of PM2.5 exposure on lung microbiome and its metabolic profile. Mice were exposed to PM2.5 through intratracheal instillation and a lung injury model was established. 16S rRNA gene sequencing indicated that PM2.5 exposure significantly altered the richness, evenness, and composition of the lung microbiome. Metabolomics profiling showed that the levels of lung metabolites were perturbed after PM2.5 exposure. The altered metabolites mainly belonged to metabolic pathways, such as the citrate cycle, glyoxylate and dicarboxylate metabolism, pyruvate metabolism, purine and pyrimidine metabolism, and valine, leucine, and isoleucine metabolism. The altered lung microbiota showed significant correlations with lung metabolites. The levels of fumaric acid negatively correlated with the relative abundance of Ruminococcaceae, Enterobacteriaceae, and Pseudomonadaceae. These results revealed that PM2.5 exposure not only significantly altered the lung microbiome composition but also perturbed a number of metabolites involved in diverse metabolic pathways. This study improves our understanding of the mechanism of lung injury after PM2.5 exposure.

Keywords: Lung injury; Metabolic pathways; Metabolomics; Microbiome; PM2.5 exposure.