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Updated: Nov 30, 2025

Measuring Carbon Content in Airway Macrophages Exposed to Carbon-Containing Particulate Matters
Published on: July 12, 2024
Fine Particulate Matter Exposure Alters Pulmonary Microbiota Composition and Aggravates Pneumococcus-Induced Lung
Yu-Wen Chen1, Shiao-Wen Li2, Chia-Der Lin3
1Department of Microbiology and Immunology, Graduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Taoyuan, Taiwan.
Abstract:
Exposure to fine particulate matter (PM) with aerodynamic diameter ≤2.5 μm (PM2. 5) is closely correlated with respiratory diseases. Microbiota plays a key role in maintaining body homeostasis including regulation of host immune status and metabolism. As reported recently, PM2. 5 exposure causes microbiota dysbiosis and thus promotes disease progression. However, whether PM2. 5 alters pulmonary microbiota distribution and aggravates bacteria-induced pathogenesis remains unknown. In this study, we used mouse experimental models of PM2. 5 exposure combined with Streptococcus pneumonia infection. We characterized the airway microbiota of bronchoalveolar lavage fluid (BALF) by sequencing the 16S rRNA V3-V4 amplicon on the Illumina MiSeq platform, followed by a combination of bioinformatics and statistical analyses. Shannon-diversity index, observed ASVs, and Fisher's diversity index indicated that microbiota richness was significantly decreased in the mice treated with either PM2. 5 or pneumococcus when compared with the control group. The genera Streptococcus, Prevotella, Leptotrichia, and Granulicatella were remarkably increased in mice exposed to PM2. 5 combined with pneumococcal infection as compared to mice with pneumococcal infection alone. Histopathological examination exhibited that a more pronounced inflammation was present in lungs of mice treated with PM2. 5 and pneumococcus than that in mouse groups exposed to either PM2. 5 or pneumococcal infection alone. Our results demonstrate that PM2. 5 alters the microbiota composition, thereby enhancing susceptibility to pneumococcal infection and exacerbating lung pathogenesis.
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