Bisphenol S exposure induces intestinal inflammation via altering gut microbiome
View abstract on PubMed
Summary
This summary is machine-generated.Bisphenol S (BPS) exposure causes intestinal inflammation in mice by disrupting gut microbiota and metabolism. Antibiotic treatment suggests gut microbes mediate this BPS toxicity, offering potential therapeutic targets.
Area Of Science
- Environmental Health
- Microbiology
- Toxicology
Background
- Bisphenol S (BPS) is a common bisphenol A substitute in food packaging.
- Concerns exist regarding BPS toxicity, but its role in gut inflammation is unclear.
Purpose Of The Study
- To investigate if gut microbiota mediates Bisphenol S (BPS)-induced intestinal inflammation.
- To elucidate the underlying mechanisms of BPS toxicity in the gut.
Main Methods
- Mouse model of Bisphenol S (BPS) exposure.
- 16S rRNA gene sequencing for gut microbiota analysis.
- LC-MS/MS untargeted metabolomics and transcriptome analysis.
- Antibiotic treatment to assess the role of gut microbiota.
Main Results
- BPS exposure induced intestinal inflammation (shortened colon, crypt distortion, apoptosis).
- BPS altered gut microbiota composition, increasing pro-inflammatory and decreasing anti-inflammatory microbes.
- BPS disrupted host and bacterial metabolism and altered intestinal gene expression.
- Antibiotic treatment ameliorated BPS-induced inflammation, confirming microbiota involvement.
Conclusions
- Bisphenol S (BPS) induces intestinal inflammation by altering gut microbiota composition and function.
- Gut microbiota plays a critical role in mediating BPS toxicity.
- Madecassic acid shows potential for preventing BPS-induced gut inflammation.
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