The role and mechanism of lung microbiota in coal mine dust-induced NLRP3 inflammasome upregulate and lung injury.

The exact molecular mechanisms of coal workers' pneumoconiosis (CWP) are still unknown. The purpose of this study is to investigate how the lung microbiota may contribute to the development of CWP. The rats were divided into five groups, including the control group, CWP group, silicosis group, CWP + antibiotic group, and CWP + MCC950 group. An animal model of CWP and silicosis was established using a non-exposed tracheal instillation method. The CWP + antibiotic group was treated with drinking and nasal drip broad-spectrum antibiotics in CWP rats, while the CWP + MCC950 group received intraperitoneal injections of NLRP3 inhibitors MCC950 in CWP rats. 16S rRNA sequencing was used to detect the lung microbiota in rats. Real-time fluorescence quantitative PCR was performed to detect the expression of NLRP3, apoptosis-associated speck-like protein (ASC), caspase-1, IL-1β, collagen I, and fibronectin. The lung microbiota of exposed to coal dust exhibits an increase in Firmicutes, Staphylococcus, and Streptococcus, and decreases in Bacteroidota, Rothia, Achromobacter, and Lactobacillus, and an increase in mRNA levels of fibrotic and inflammatory markers. Antibiotic intervention and MCC950 had consistent impacts on the predominant microbiota in the lungs and the changes are essentially in opposition to the trends found in the CWP and control groups, whereas mRNA levels of fibrotic and inflammatory markers reduced. The richness of some prominent bacterial communities changed as a result of coal dust exposure, which could be a contributing factor to the inflammation and fibrosis caused by coal dust. Lung microbiota may serve as a key pathogenic mechanism in CWP.