Exposure to concentrated ambient PM2.5 alters the composition of gut microbiota in a murine model
JournalParticle and Fibre Toxicology
PublisherBioMed Central Ltd.
MetadataShow full item record
AbstractBackground: Exposure to ambient fine particulate matter (PM2.5) correlates with abnormal glucose homeostasis, but the underlying biological mechanism has not been fully understood. The gut microbiota is an emerging crucial player in the homeostatic regulation of glucose metabolism. Few studies have investigated its role in the PM2.5 exposure-induced abnormalities in glucose homeostasis. Methods: C57Bl/6J mice were exposed to filtered air (FA) or concentrated ambient PM2.5 (CAP) for 12 months using a versatile aerosol concentration enrichment system (VACES) that was modified for long-term whole-body exposures. Their glucose homeostasis and gut microbiota were examined and analysed by correlation and mediation analysis. Results: Intraperitoneal glucose tolerance test (IPGTT) and insulin tolerance test (ITT) showed that CAP exposure markedly impaired their glucose and insulin tolerance. Faecal microbiota analysis demonstrated that the impairment in glucose homeostasis was coincided with decreased faecal bacterial ACE and Chao-1 estimators (the indexes of community richness), while there was no significant change in all faecal fungal alpha diversity estimators. The Pearson's correlation analyses showed that the bacterial richness estimators were correlated with glucose and insulin tolerance, and the mediation analyses displayed a significant mediation of CAP exposure-induced glucose intolerance by the alteration in the bacterial Chao-1 estimator. LEfSe analyses revealed 24 bacterial and 21 fungal taxa differential between CAP- and FA-exposed animals. Of these, 14 and 20 bacterial taxa were correlated with IPGTT AUC and ITT AUC, respectively, and 5 fungal taxa were correlated with abnormalities in glucose metabolism. Conclusions: Chronic exposure to PM2.5 causes gut dysbiosis and may subsequently contribute to the development of abnormalities in glucose metabolism. Copyright 2018 The Author(s).
SponsorsThis work was supported by the National Institutes of Health (R01ES024516 to ZY), the American Heart Association (13SDG17070131 to ZY), the National Natural Science Foundation of China (Grant No. 81270342 to ZY and 81500216 to MC), Shanghai Pujiang Program (17PJ1401300 to YX), and Program for Professor of Special Appointment (Eastern Scholar) at Shanghai Institutions of Higher Learning (SSF201008 to ZY)
Identifier to cite or link to this itemhttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85045517791&doi=10.1186%2fs12989-018-0252-6&partnerID=40&md5=c334ef0b53ba9fd15fe7da72b2851236; http://hdl.handle.net/10713/9477