Fine Particulate Matter Exposure Alters Pulmonary Microbiota Composition and Aggravates Pneumococcus-Induced Lung Pathogenesis

Abstract

Exposure to fine particulate matter (PM) with aerodynamic diameter ≤2.5 µm (PM 2.5) 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, PM 2.5 exposure causes microbiota dysbiosis and thus promotes disease progression. However, whether PM 2.5 alters pulmonary microbiota distribution and aggravates bacteria-induced pathogenesis remains unknown. In this study, we used mouse experimental models of PM 2.5 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 PM 2.5 or pneumococcus when compared with the control group. The genera Streptococcus, Prevotella, Leptotrichia, and Granulicatella were remarkably increased in mice exposed to PM 2.5 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 PM 2.5 and pneumococcus than that in mouse groups exposed to either PM 2.5 or pneumococcal infection alone. Our results demonstrate that PM 2.5 alters the microbiota composition, thereby enhancing susceptibility to pneumococcal infection and exacerbating lung pathogenesis.

The Effects of Immunosuppression on the Lung Microbiome and Metabolites in Rats

“…Consequently, pathogenic bacterial physiology must be adapted to these different physiological conditions to ensure the expression of adaptive and virulence factors ( Hartel et al, 2012 ). The microbial community changes dynamically depending on the lung condition, followed by pneumococcal infection ( Chen et al, 2020 ). In this paper, we found that L -Aspartic acid, Methylmalonate, N -Acetyl-α- D -glucosamine 1-phosphate, Theophylline, and dAMP, which are the main intermediates of metabolic pathways, were positively related to the abundance of Streptococcaceae and Enterobacteriaceae .…”

E-Cigarette Use, Cigarette Use, and Sex Modify the Nasal Microbiome and Nasal Host-Microbiota Interactions

“…As a whole, our results support and expand on the previously published notion that exposure to inhaled toxicants, including tobacco products, can influence the respiratory microbiome. 23,83,84 The novel, robust computational approach in terms of pairwise log ratios that we applied allowed us to uncover both exposure-and sex-dependent effects on nasal mucosal host defense responses using straightforward, non-invasive sampling of the upper respiratory tract of human subjects. Importantly, we were able to integrate 16S sequencing data with expression of soluble immune mediators to understand interactions between the nasal microbiome and host milieu by appropriately handling the sparse, compositional data generated by 16S sequencing, accounting for inter-individual variability between subjects' mediator levels, and selecting for features that were most important for separating classes, resulting in interpretable, biologically meaningful results.…”

Air Pollution and the Airways: Lessons from a Century of Human Urbanization

“…Last but not least, the microbiome present in the lungs should also be mentioned. PM exposure, even subchronic, in mice leads to alterations both in the lung microbiome as well as in the gut microbiome (decreased microbiome richness) leading to lung and intestinal damage and systemic inflammation [125,126]. Secondly, microbiota dysbiosis leads to enhanced susceptibility to other bacterial infections in the lung, such as a pneumococcal infection [126].…”

“…PM exposure, even subchronic, in mice leads to alterations both in the lung microbiome as well as in the gut microbiome (decreased microbiome richness) leading to lung and intestinal damage and systemic inflammation [125,126]. Secondly, microbiota dysbiosis leads to enhanced susceptibility to other bacterial infections in the lung, such as a pneumococcal infection [126]. Bacteria can also be used as a therapeutic tool, and this applies also to PM-induced lung allergic inflammation.…”