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Hepatic injury and ileitis associated with gut microbiota dysbiosis in mice upon F-53B exposure.

Author information

Affiliations

  • 1. Joint International Research Laboratory of Environment and Health, Ministry of Education, Guangdong Provincial Engineering Technology Research Center of Environmental Pollution and Health Risk Assessment, Department of Occupational and Environmental Health, School of Public Health, Sun Yat-sen University, Guangzhou, 510080, China.
      Authors
    • Li S 1
    • Wu L 1
    • Zeng H 1
    • Zhang J 1
    • Qin S 1
    • Liang LX 1
    • Meng WJ 1
    • Chen XY 1
    • Wu QZ 1
    • Lin LZ 1
    • Dong GH 1
    • Zeng XW 1
    (12 authors)
  • 2. Department of Psychology Umeå University, Umeå, SE-90187, Sweden.
      Authors
    • Andersson J 2
    (1 author)
  • 3. Center for Environmental and Human Toxicology, Department of Environmental and Global Health, College of Public Health and Health Professions, University of Florida, Gainesville, FL 32611, United States. Electronic address: ude.lfu@uohc.w.
      Authors
    • Chou WC 3
    (1 author)

ORCIDs linked to this article

Environmental Research, 01 Feb 2024, 248:118305
https://doi.org/10.1016/j.envres.2024.118305 PMID: 38307183 

Abstract 

Chlorinated polyfluorinated ether sulfonate (F-53B), a substitute of perfluorooctane sulfonic acid (PFOS), has attracted significant attention for its link to hepatotoxicity and enterotoxicity. Nevertheless, the underlying mechanisms of F-53B-induced enterohepatic toxicity remain incompletely understood. This study aimed to explore the role of F-53B exposure on enterohepatic injury based on the gut microbiota, pathological and molecular analysis in mice. Here, we exposed C57BL/6 mice to F-53B (0, 4, 40, and 400 μg/L) for 28 days. Our findings revealed a significant accumulation of F-53B in the liver, followed by small intestines, and feces. In addition, F-53B induced pathological collagen fiber deposition and lipoid degeneration, up-regulated the expression of fatty acid β-oxidation-related genes (PPARα and PPARγ, etc), while simultaneously down-regulating pro-inflammatory genes (Nlrp3, IL-1β, and Mcp1) in the liver. Meanwhile, F-53B induced ileal mucosal barrier damage, and an up-regulation of pro-inflammatory genes and mucosal barrier-related genes (Muc1, Muc2, Claudin1, Occludin, Mct1, and ZO-1) in the ileum. Importantly, F-53B distinctly altered gut microbiota compositions by increasing the abundance of Akkermansia and decreasing the abundance of Prevotellaceae_NK3B31_group in the feces. F-53B-altered microbiota compositions were significantly associated with genes related to fatty acid β-oxidation, inflammation, and mucosal barrier. In summary, our results demonstrate that F-53B is capable of inducing hepatic injury, ileitis, and gut microbiota dysbiosis in mice, and the gut microbiota dysbiosis may play an important role in the F-53B-induced enterohepatic toxicity.

Full text links 

Read article at publisher's site: https://doi.org/10.1016/j.envres.2024.118305

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Funding 

Funders who supported this work.

National Natural Science Foundation of China (4)

Natural Science Foundation of Guangdong Province (2)

Sun Yat-Sen University