Perinatal Bisphenol A Exposure Induces Chronic Inflammation in Rabbit Offspring via Modulation of Gut Bacteria and Their Metabolites

Metabolome Dysbiosis Endocrine disruptor Intestinal Permeability
DOI: 10.1128/msystems.00093-17 Publication Date: 2017-10-11T00:40:29Z
ABSTRACT
Bisphenol A (BPA) accumulates in the maturing gut and liver utero is known to alter bacterial profiles offspring. Gut dysbiosis may contribute chronic colonic systemic inflammation. We hypothesized that perinatal BPA exposure-induced intestinal (and liver) inflammation offspring due alterations microbiome metabolome. The 16S rRNA amplicon sequencing analysis revealed differences beta diversity with a significant reduction relative abundances of short-chain fatty acid (SCFA) producers such as Oscillospira Ruminococcaceae exposure. Furthermore, exposure reduced fecal SCFA levels increased lipopolysaccharide (LPS) levels. exposure-increased permeability was ameliorated by addition vitro. Metabolic fingerprints global metabolism amino metabolism. Thus, our findings indicate cause altered metabolite profiles, particularly leading colon IMPORTANCE Emerging evidence suggests environmental toxicants influence inflammation-promoted disease susceptibility during early life. BPA, an endocrine disruptor, can transfer across placenta accumulate fetal liver. However, underlying mechanisms for BPA-induced are not fully elucidated. In this report, we show how rabbits alters microbiota their which leads well measured elevated serum Also, metabolites (short-chain acids [SCFA]) permeability-three common biomarkers diseases. addition, showed study results suggest correcting toxicant-induced life reduce risk diseases later
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