Lung microbiome and transcriptome reveal mechanisms underlying PM2.5 induced pulmonary fibrosis

Airborne fine particulate matter (PM2.5 ) is considered to be a risk factor for lung fibrosis, and therefore, it has attracted public attention due to its various physicochemical features and its adverse effects on health. However, little remains to be known regarding the mechanism of PM2.5 -induced pulmonary fibrosis. The lung microbiota may be a potential fac-tor involved in the adverse outcomes of pulmonary fibrosis. Meanwhile, miRNAs are thought to be key regulators that participate in the complex interplay between the host and the microbiota. Hence, to investigate the potential mechanisms of pulmonary fibrosis, and to explore the impact of PM2.5 -induced alterations in miRNAs and the lung microbiota and possible interaction patterns in mice models, we took advantage of 16S rDNA gene sequencing, miRNAs sequencing (miRNAs-Seq), and mining of public databases profiling. The results of 16S rDNA analysis showed that PM2.5 interfered with the microbial community composition, resulting in Proteobacteria becoming an additional dominant phylum. In addition, differentially expressed miRNAs were enriched in HIF-1 signaling, the IL-17 signaling, as well as Th17 cell differentiation pathways, which are closely related to microbial functional pathways. Significantly, a target miRNA, miR-149-5p, may be a key factor triggering the MAPK signal pathway related to pulmonary fibrosis and disturbing the homeostasis of lung bacterial flora. These results indicate that PM2.5 may lead to interaction be-tween lung microbiota dysbiosis and an imbalance of miRNA levels to forma vicious cycle that promotes lung fibro-genesis. The current study provides new insights into the progression of pulmonary fibrosis.

Automated summary

Airborne fine particulate matter (PM2.5) is considered a risk factor for lung fibrosis. This study investigated the potential mechanisms of PM2.5-induced pulmonary fibrosis and the impact of PM2.5-induced alterations in miRNAs and the lung microbiota in mice models. The results showed that PM2.5 affected the microbial community composition and differentially expressed miRNAs enriched in pathways related to microbial functions. A target miRNA, miR-149-5p, may be a key factor triggering pulmonary fibrosis. The study provides new insights into the progression of pulmonary fibrosis.