Objective: Perfluorooctanesulfonic acid (PFOS), a persistent environmental pollutant, is implicated in immune dysregulation. Rising inflammatory bowel disease (IBD) incidence parallels environmental contamination, yet PFOS's role in gut inflammation remains unclear. Its immunotoxicity may disrupt intestinal homeostasis via barrier dysfunction or cytokine imbalance, but molecular targets and pathways linking PFOS to IBD pathogenesis require elucidation to inform risk mitigation strategies.
Methods: This study aims to elucidate the mechanism of action of PFOS in the development and progression of IBD. Additionally, relevant PFOS targets and IBD-associated genes were screened using databases such as results indicate that PFOS is significantly associated with key pathways involved in IBD, and it can specifically bind to crucial IBD proteins like albumin, epidermal growth factor, fos proto-oncogene, and interleukin-10.
Results: The study suggests that PFOS may contribute to the pathogenesis of IBD by interfering with key proteins and signaling pathways, highlighting its potential health risks, and providing a theoretical basis for subsequent clinical research and prevention strategies.
Conclusion: In conclusion, this study has untangled the potential mechanistic link between PFOS exposure and inflammatory bowel disease, offering a novel perspective for environmental health science and public health policies and profound implications.
Keywords: inflammatory bowel disease; inflammatory infiltration; perfluorooctane sulfonate.
Copyright © 2025 The Author(s). Published by Wolters Kluwer Health, Inc.