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Maternal immune activation perturbs intestinal niche through microbial glycerophospholipids and drives offspring behavioral abnormalities

ABSTRACT: Using a mouse MIA model induced by prenatal exposure to Toxoplasma gondii soluble tachyzoite antigen (STAg), we reveal that maternal gut dysbiosis, characterized by increased Firmicutes and Actinobacteria, drives offspring behavioral deficits. This dysbiosis disrupts intestinal barrier integrity and induces metabolic and inflammatory dysregulation, characterized by elevated M1 macrophages and IL-6, alongside a pronounced accumulation of the glycerophospholipid. metabolite

ORGANISM(S): Mus Musculus

SUBMITTER: Zhipeng Xu

PROVIDER: PXD075246 | iProX | Wed Mar 04 00:00:00 GMT 2026

REPOSITORIES: iProX

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Maternal immune activation perturbs intestinal niche through microbial glycerophospholipids and drives offspring behavioral abnormalities.

Chang Hao H Zhu Xinyi X Shen Chunxiang C Xu Xuejun X Ni Yangyue Y Zhang Yu Y Yan Juming J Xue Jingyao J Li Chi C Qin Qi Q Hai Kexin K Hou Min M Zhou Zikai Z Ji Minjun M Xu Zhipeng Z

Cell reports 20260331 4

Maternal immune activation (MIA) contributes to neurodevelopmental deficits in offspring, yet the prenatal mechanisms remain elusive. Here, using a mouse MIA model induced by prenatal exposure to Toxoplasma gondii soluble tachyzoite antigen (STAg), we reveal that maternal gut dysbiosis, characterized by increased Firmicutes and Actinobacteria, drives offspring behavioral deficits. This dysbiosis disrupts intestinal barrier integrity and induces metabolic and inflammatory dysregulation, character ...[more]

PMID: 41926285

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