4.8 Article

Exposure to concentrated ambient PM2.5 (CAPM) induces intestinal disturbance via inflammation and alternation of gut microbiome

期刊

ENVIRONMENT INTERNATIONAL
卷 161, 期 -, 页码 -

出版社

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.envint.2022.107138

关键词

Inhalation exposure; Ambient PM2.5; Inflammation; Intestinal microbiome; Correlations

资金

  1. China National Natural Science Foundation [22122601, 92043301]
  2. Open Research Fund Program of State Environmental Protection Key Laboratory of Food Chain Pollution Control
  3. Shanghai Natural Science Foundation [20ZR1404300, 21DZ1202300, 21230712800]

向作者/读者索取更多资源

Air pollution, particularly the presence of fine particulate matter (PM2.5), has been linked to intestinal diseases. In this study, researchers investigated the effects of ambient PM2.5 on intestinal tissue and microbiome through inhalation exposure. The results showed that exposure to high levels and prolonged periods of concentrated ambient PM2.5 (CAPM) damaged the colon's mucous layer, altered the expression of genes related to tight junction and inflammation, and caused changes in the composition of intestinal microbiome. The study also found that the alteration of gut microbiome induced by CAPM exposure was related to intestinal inflammation, suggesting a potential mechanism for PM2.5-induced intestinal diseases. These findings contribute to our understanding of the toxicology and health effects of ambient PM2.5.
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 micmbiome 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, IL10 and IL-1 beta) 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, Bactemidetes was greatly decreased, while Proteobacteria was increased after exposure to CAPM, comparing with exposure to FA. At the genus level, Clostridium XIVa, 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.

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