Abstract
BackgroundAmbient particulate matter exposure has been shown to increase the risks of respiratory diseases. However, the role of the lung microbiome and the immune response to inhaled particulate matter are largely unexplored. We studied the influence of biomass fuel and motor vehicle exhaust particles on the lung microbiome and pulmonary immunologic homeostasis in rats.MethodsFifty-seven Sprague–Dawley rats were randomly divided into clean air (CON), biomass fuel (BMF), and motor vehicle exhaust (MVE) groups. After a 4-week exposure, the microbial composition of the lung was assessed by 16S rRNA pyrosequencing, the structure of the lung tissue was assessed with histological analysis, the phagocytic response of alveolar macrophages to bacteria was determined by flow cytometry, and immunoglobulin concentrations were measured with commercial ELISA kits.ResultsThere was no significant difference in lung morphology between the groups. However, the BMF and MVE groups displayed greater bacterial abundance and diversity. Proteobacteria were present in higher proportions in the MVE group, and 12 bacterial families differed in their relative abundances between the three groups. In addition, particulate matter exposure significantly increased the capacity of alveolar macrophages to phagocytose bacteria and induced changes in immunoglobulin levels.ConclusionWe demonstrated that particulate matter exposure can alter the microbial composition and change the pulmonary immunologic homeostasis in the rat lung.
Highlights
Ambient particulate matter exposure has been shown to increase the risks of respiratory diseases
Phagocytosis by Alveolar macrophages (AM) following Particulate matter (PM) exposure There were no significant differences in total bronchoalveolar lavage fluid (BALF) cell counts between the PM exposure group and control group, but the BALF macrophage counts increased in the biomass fuel (BMF) group compared with the control group (p = 0.045) (Fig. 2)
AMs from the BMFexposed group exhibited an increased capacity to ingest S. aureus (p = 0.012), but did not differ from AMs derived from control rats in their capacity to ingest S. pneumoniae (p = 0.097) (Fig. 3)
Summary
Ambient particulate matter exposure has been shown to increase the risks of respiratory diseases. The role of the lung microbiome and the immune response to inhaled particulate matter are largely unexplored. Inhaled ambient PM represents important environmental exposures that have been linked to death and disease [1, 2]. Emerging epidemiological evidence suggests that these exposures increase the risks of respiratory diseases [3,4,5,6]. Research on PM has mostly focused on the lung inflammatory response to inhalation, as this is considered the primary impact of PM exposure [7,8,9,10]. Previous studies have found that airborne PM exposure alters the gut microbiome and induces acute and chronic inflammatory responses in the
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