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Exposure to concentrated ambient PM2.5 (CAPM) induces intestinal disturbance via inflammation and alternation of gut microbiome
Graphical abstract Display Omitted
Highlightss Exposure to CAPM induced intestinal damage and inflammation. Exposure to CAPM altered gut microbiota composition. Exposure time and CAPM changed the metabolic function of gut microbiota. Intestinal inflammation was correlated to the change of certain gut microbiota.
Abstract Air pollution causes a great disease burden worldwide. Recent evidences suggested that PM2.5 contributes to intestinal disease. The objective of present study was to investigate the influence of ambient PM2.5 on intestinal tissue and microbiome via whole-body inhalation exposure. The results showed that high levels and prolonged periods exposure to concentrated ambient PM2.5 (CAPM) could destroy the mucous layer of the colon, and significantly alter the mRNA expression of tight junction (Occludin and ZO-1) and inflammation-related (IL-6, IL-10 and IL-1β) genes in the colon, comparing with exposure to the filtered air (FA). The composition of intestinal microbiome at the phylum and genus levels also varied along with the exposure time and PM2.5 levels. At the phylum level, Bacteroidetes was greatly decreased, while Proteobacteria was increased after exposure to CAPM, comparing with exposure to FA. At the genus level, Clostridium XlVa, Akkermansia and Acetatifactor, were significantly elevated exposure to CAPM, comparing with exposure to FA. Our results also indicated that high levels and prolonged periods exposure to CAPM altered metabolic functional pathways. The correlation analysis showed that the intestinal inflammation was related to the alteration of gut microbiome induced by CAPM exposure, which may be a potential mechanism that elucidates PM2.5-induced intestinal diseases. These results extend our knowledge on the toxicology and health effects of ambient PM2.5.
Exposure to concentrated ambient PM2.5 (CAPM) induces intestinal disturbance via inflammation and alternation of gut microbiome
Graphical abstract Display Omitted
Highlightss Exposure to CAPM induced intestinal damage and inflammation. Exposure to CAPM altered gut microbiota composition. Exposure time and CAPM changed the metabolic function of gut microbiota. Intestinal inflammation was correlated to the change of certain gut microbiota.
Abstract Air pollution causes a great disease burden worldwide. Recent evidences suggested that PM2.5 contributes to intestinal disease. The objective of present study was to investigate the influence of ambient PM2.5 on intestinal tissue and microbiome via whole-body inhalation exposure. The results showed that high levels and prolonged periods exposure to concentrated ambient PM2.5 (CAPM) could destroy the mucous layer of the colon, and significantly alter the mRNA expression of tight junction (Occludin and ZO-1) and inflammation-related (IL-6, IL-10 and IL-1β) genes in the colon, comparing with exposure to the filtered air (FA). The composition of intestinal microbiome at the phylum and genus levels also varied along with the exposure time and PM2.5 levels. At the phylum level, Bacteroidetes was greatly decreased, while Proteobacteria was increased after exposure to CAPM, comparing with exposure to FA. At the genus level, Clostridium XlVa, Akkermansia and Acetatifactor, were significantly elevated exposure to CAPM, comparing with exposure to FA. Our results also indicated that high levels and prolonged periods exposure to CAPM altered metabolic functional pathways. The correlation analysis showed that the intestinal inflammation was related to the alteration of gut microbiome induced by CAPM exposure, which may be a potential mechanism that elucidates PM2.5-induced intestinal diseases. These results extend our knowledge on the toxicology and health effects of ambient PM2.5.
Exposure to concentrated ambient PM2.5 (CAPM) induces intestinal disturbance via inflammation and alternation of gut microbiome
Xie, Shanshan (author) / Zhang, Caihong (author) / Zhao, Jinzhuo (author) / Li, Dan (author) / Chen, Jianmin (author)
2022-02-05
Article (Journal)
Electronic Resource
English
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