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Microbial tryptophan-IPA axis mediates 6:2 chlorinated polyfluorinated ether sulfonate (6:2Cl-PFESA)-induced
Xingyue Shan1, Lan Shi2, Tailin Zhu3
1Shanghai Key Laboratory of Brain Functional Genomics (Ministry of Education), School of Life Sciences, East China Normal University, Shanghai 200062, China; Ministry of Education-Shanghai Key Laboratory of Children's Environmental Health, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China.
Environment International
|July 21, 2026
Summary
Exposure to substitute PFAS like F-53B impairs memory in young mice by disrupting the gut-brain axis. Supplementing with indole-3-propionic acid (IPA) reversed these neurobehavioral effects, highlighting the gut microbiome
Area of Science:
- Environmental Science
- Neuroscience
- Toxicology
Background:
- Chlorinated polyfluoroalkyl ether sulfonic acids (Cl-PFESAs) are emerging contaminants and replacements for PFOS.
- Neurobehavioral effects of early-life Cl-PFESA exposure are not well understood.
Purpose of the Study:
- To investigate the neurobehavioral toxicity of F-53B (a 6:2Cl-PFESA) in juvenile mice.
- To elucidate the underlying gut-brain axis mechanisms, including microbiome and metabolic alterations.
Main Methods:
- Oral exposure of male C57BL/6J mice to F-53B (0.1 or 1 mg/kg/day) during juvenility.
- Behavioral assessments (recognition memory, social novelty, locomotor activity, anxiety, working memory).
- Analysis of intestinal barrier integrity, gut microbiota, serum inflammatory markers, hippocampal neuroinflammation, and tryptophan metabolism.
Main Results:
- F-53B selectively impaired recognition memory and social novelty preference.
- Exposure compromised intestinal barrier integrity, increased LPS, and induced systemic inflammation.
- Hippocampal neuroinflammation and synaptic changes were observed, linked to microbiome and tryptophan metabolism disruption.
- Indole-3-propionic acid (IPA) supplementation rescued behavioral deficits and attenuated gut-brain inflammatory pathways.
Conclusions:
- A microbiota-tryptophan metabolite-gut barrier-inflammation axis mediates F-53B-induced neurobehavioral dysfunction.
- Microbiota-derived metabolites like IPA are critical modulators of PFAS neurotoxicity.
- Early-life exposure to substitute PFAS poses significant neurodevelopmental risks.
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