Gut Microbiota-Associated Suppression of Intestinal β-Catenin Signaling Contributes to Barrier Dysfunction and Hepatic Pyroptosis Following SCCPs Exposure.

Authors

Donglei Huang, Wen Zhang, Xiao Wang, Liting Gan, Hongcai Liu, Rongzhu Liu, Mengjiao Yu, Jiang Qiu, Hanrui Liu, Luyao Jiang, Jinyu Tang, Jiaxin Liu, Xinyuan Zhao, Haiping Gao, Ya Zhang, Jing Xiao

Published in

Toxicology. Pages 154581. Sep 05, 2026. Epub Sep 05, 2026.

Abstract

Short-chain chlorinated paraffins (SCCPs), as persistent organic pollutants, pose potential health threats, yet their toxicological mechanisms remain incompletely elucidated. This study demonstrates that exposure to SCCPs can induce liver injury in mice. Specifically, SCCPs interfere with the expression of intestinal tight junction proteins in a gut microbiota-dependent manner, leading to increased intestinal permeability and a subsequent elevation of serum lipopolysaccharide (LPS) levels. LPS activates the Toll-like Receptor 4 (TLR4)/Nuclear Factor kappa-B (NF-κB) signaling pathway and influences macrophage polarization, thereby inducing pyroptosis-related signaling in the liver. Further investigation reveals that the gut microbiota dysbiosis induced by SCCPs exposure disrupts the intestinal barrier and induces hepatotoxicity in association with downregulating the Wnt/β-catenin pathway. In summary, this study provides evidence that SCCPs contribute to gut-liver axis disruption through gut microbiota dysbiosis and suppression of the Wnt/β-catenin pathway, providing new insights into their toxicological effects.

PMID:
42700885
Bibliographic data and abstract were imported from PubMed on 06 Sep 2026.

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