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Perinatal Bisphenol A Exposure Induces Chronic Inflammation in Rabbit Offspring via Modulation of Gut Bacteria and
Lavanya Reddivari1, D N Rao Veeramachaneni2, William A Walters3
1Department of Plant Science, The Pennsylvania State University, University Park, Pennsylvania, USA.
Msystems
|October 17, 2017
Summary
Perinatal exposure to Bisphenol A (BPA) alters gut bacteria and metabolites, causing inflammation and increased gut permeability in offspring. Restoring gut bacteria may reduce chronic disease risk.
Area of Science:
- Environmental Health
- Microbiology
- Toxicology
Background:
- Bisphenol A (BPA) is an endocrine disruptor that crosses the placenta, accumulating in fetal gut and liver.
- BPA exposure in early life is linked to gut dysbiosis and inflammation, but mechanisms remain unclear.
Purpose of the Study:
- To investigate if perinatal BPA exposure causes intestinal and liver inflammation in offspring due to microbiome and metabolome alterations.
- To explore the role of short-chain fatty acids (SCFAs) in BPA-induced gut inflammation and permeability.
Main Methods:
- 16S rRNA amplicon sequencing to analyze gut microbiota composition.
- Measurement of fecal short-chain fatty acids (SCFAs) and serum lipopolysaccharide (LPS) levels.
- In vitro assessment of SCFA's effect on intestinal permeability.
Main Results:
- BPA exposure reduced bacterial diversity and SCFA-producing bacteria (e.g., Oscillospira, Ruminococcaceae).
- Fecal SCFA levels decreased, while serum LPS levels increased, indicating impaired gut barrier function.
- Metabolic profiling revealed alterations in global and amino acid metabolism.
- In vitro, SCFAs ameliorated BPA-induced intestinal permeability.
Conclusions:
- Perinatal BPA exposure induces gut dysbiosis and metabolic changes, leading to increased intestinal permeability and inflammation.
- Reduced SCFAs and altered gut microbiota are key mediators of BPA's adverse effects.
- Targeting gut dysbiosis and restoring SCFAs early in life may mitigate risks of chronic diseases associated with environmental toxicants.