ArticleEnvironmental pollution (Barking, Essex : 1987)2026
Oral exposure to perfluorooctanoic acid disrupts the microbiota-gut-liver axis and enhances the severity of chemically induced colitis in mice.
Article in Environmental pollution (Barking, Essex : 1987), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- The Gut-Skin Axis in Atopic Dermatitis and Inflammatory Bowel Disease: Mechanisms, Microbiota, and Therapeutic Implications.Journal of personalized medicine · 2026Review
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Authors and funding
14 authors.
Funding
Abstract
Inflammatory bowel diseases (IBD) affect millions of patients worldwide and impair quality of life. Although genetic and environmental factors are known to disrupt the gastrointestinal (GI) epithelial barrier and increase susceptibility to IBD, the precise contribution of specific environmental exposures remains unclear. Per- and polyfluoroalkyl substances (PFAS), or "forever chemicals," are widely used in consumer products and contaminate food and water sources, resulting in chronic oral exposure worldwide. Perfluorooctanoic acid (PFOA), a common PFAS, has been epidemiologically associated with the development of IBD, particularly in older adults. Here, we assessed the effects of oral PFOA exposure on the GI tract, liver, and susceptibility to colitis. C57BL/6 mice were exposed to PFOA (0.1 or 1.0 mg/kg) beginning at weaning (postnatal day [P]21) for a time course of 4 or 8 weeks. GI physiology/pathology (Ussing chambers; histology), expression of pro-inflammatory cytokines (qPCR), microbiota composition (16S sequencing), bile acid production (qPCR; LC/MS), and liver pathology (histology) were assessed. Colitis susceptibility was evaluated in genetically predisposed (IL10 knockout) mice, and in chemically induced (dextran sodium sulfate [DSS]) mouse models following PFOA exposure (8 weeks at 1.0 mg/kg). Oral PFOA exposure increased intestinal permeability, mildly increased cytokine expression, altered gut microbiota composition, disrupted liver and serum bile acids, and caused hepatic hypertrophy in the high dose and longer exposure. Although PFOA did not increase disease susceptibility in genetically predisposed IL10 KO mice, it significantly worsened DSS-induced colitis, but only in male mice. Together, these findings demonstrate that early-life PFOA exposure disrupts the gut-liver axis and may contribute to colitis development in a sex-dependent manner.
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