Wang Fan, Cheng Baolong, Wu Wei, Chen Yu, Dai Jiaxin, Li Yaoping
Department of Colorectal Surgery, Shanxi Provincial People's Hospital, Fifth Clinical Medical College of Shanxi Medical University, Taiyuan, Shanxi, China.
Shanxi Medical University School and Hospital of Stomatology, Taiyuan, Shanxi, China.
Int J Surg. 2025 Aug 1;111(8):5150-5161. doi: 10.1097/JS9.0000000000002638. Epub 2025 Jun 10.
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.
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.
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.
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.
全氟辛烷磺酸（PFOS）是一种持久性环境污染物，与免疫调节异常有关。炎症性肠病（IBD）发病率的上升与环境污染同步，但PFOS在肠道炎症中的作用仍不清楚。其免疫毒性可能通过屏障功能障碍或细胞因子失衡破坏肠道稳态，但将PFOS与IBD发病机制联系起来的分子靶点和途径需要阐明，以为风险缓解策略提供依据。
本研究旨在阐明PFOS在IBD发生发展过程中的作用机制。此外，利用诸如……等数据库筛选相关的PFOS靶点和IBD相关基因。结果表明，PFOS与IBD相关的关键途径显著相关，并且它可以特异性结合关键的IBD蛋白，如白蛋白、表皮生长因子、原癌基因fos和白细胞介素-10。
该研究表明，PFOS可能通过干扰关键蛋白和信号通路促进IBD的发病机制，突出了其潜在的健康风险，并为后续临床研究和预防策略提供了理论依据。
总之，本研究理清了PFOS暴露与炎症性肠病之间潜在的机制联系，为环境卫生科学和公共卫生政策提供了新的视角，并具有深远意义。
