| Autor: |
Wang, Tingting, Chen, Beidi, Luo, Mingcui, Xie, Lulu, Lu, Mengxi, Lu, Xiaoqian, Zhang, Shuai, Wei, Liyi, Zhou, Xinli, Yao, Baozhen, Wang, Hui, Xu, Dan |
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| Zdroj: |
Microbiome; 11/7/2023, Vol. 11 Issue 1, p1-23, 23p |
| Abstrakt: |
Background: Autism spectrum disorder (ASD) has been associated with intrauterine growth restriction (IUGR), but the underlying mechanisms are unclear. Results: We found that the IUGR rat model induced by prenatal caffeine exposure (PCE) showed ASD-like symptoms, accompanied by altered gut microbiota and reduced production of indole 3-propionic acid (IPA), a microbiota-specific metabolite and a ligand of aryl hydrocarbon receptor (AHR). IUGR children also had a reduced serum IPA level consistent with the animal model. We demonstrated that the dysregulated IPA/AHR/NF-κB signaling caused by disturbed gut microbiota mediated the hippocampal microglia hyperactivation and neuronal synapse over-pruning in the PCE-induced IUGR rats. Moreover, postnatal IPA supplementation restored the ASD-like symptoms and the underlying hippocampal lesions in the IUGR rats. Conclusions: This study suggests that the microbiota-IPA-brain axis regulates ASD susceptibility in PCE-induced IUGR offspring, and supplementation of microbiota-derived IPA might be a promising interventional strategy for ASD with a fetal origin. 21xhjpDoyB4JmdH7kH-NGn Video Abstract [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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