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Bisphenol S exposure induces intestinal inflammation: An integrated metabolomic and transcriptomic study
Junjie Ao1, Yongjie Liu1, Weifeng Tang1
1Ministry of Education-Shanghai Key Laboratory of Children's Environmental Health, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200092, China.
Chemosphere
|January 3, 2022
Summary
Bisphenol S (BPS) exposure harms human colon cells by increasing inflammation and damaging gut barrier integrity. This study reveals potential disruptions to the gut-brain axis, linking environmental pollutants to intestinal issues.
Area of Science:
- Environmental Health
- Toxicology
- Gastroenterology
Background:
- Bisphenol A (BPA) replacement, Bisphenol S (BPS), raises health concerns.
- Limited data exists on BPS toxicity to the human digestive system, particularly the intestine.
Purpose of the Study:
- Investigate BPS effects on human colon mucosal epithelial cells (NCM460).
- Elucidate the mechanisms underlying BPS-induced intestinal toxicity.
Main Methods:
- Exposed NCM460 cells to BPS.
- Analyzed pro-inflammatory cytokine production (TNF-α, IFN-γ, IL-17A).
- Assessed tight junction protein expression (Claudin1, ZO1).
- Conducted multi-omics (metabolomics, transcriptomics) analysis.
Main Results:
- BPS significantly increased pro-inflammatory cytokines (TNF-α, IFN-γ, IL-17A).
- BPS exposure disrupted tight junctions by down-regulating Claudin1 and ZO1.
- Multi-omics revealed increased neurotransmitters and activation of the 'glutamatergic synapse' pathway, with up-regulated l-glutamine.
Conclusions:
- BPS exposure induces inflammation and tight junction destruction in colon cells.
- BPS may disrupt the gut-brain axis, contributing to intestinal inflammation.
- Findings offer insights into environmental pollutants' role in intestinal disease development.
