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Amelioration of Maternal Immune Activation-Induced Autism Relevant Behaviors by Gut Commensal Parabacteroides goldsteinii

Autism spectrum disorder (ASD) is characterized by cognitive inflexibility and social deficits. Probiotics have been demonstrated to play a promising role in managing the severity of ASD. However, there are no effective probiotics for clinical use. Identifying new probiotic strains for ameliorating...

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Autores principales: Lin, Tzu-Lung, Lu, Cha-Chen, Chen, Ting-Wen, Huang, Chih-Wei, Lu, Jang-Jih, Lai, Wei-Fan, Wu, Ting-Shu, Lai, Chih-Ho, Lai, Hsin-Chih, Chen, Ya-Lei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
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Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9657948/
https://www.ncbi.nlm.nih.gov/pubmed/36361859
http://dx.doi.org/10.3390/ijms232113070
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author Lin, Tzu-Lung
Lu, Cha-Chen
Chen, Ting-Wen
Huang, Chih-Wei
Lu, Jang-Jih
Lai, Wei-Fan
Wu, Ting-Shu
Lai, Chih-Ho
Lai, Hsin-Chih
Chen, Ya-Lei
author_facet Lin, Tzu-Lung
Lu, Cha-Chen
Chen, Ting-Wen
Huang, Chih-Wei
Lu, Jang-Jih
Lai, Wei-Fan
Wu, Ting-Shu
Lai, Chih-Ho
Lai, Hsin-Chih
Chen, Ya-Lei
author_sort Lin, Tzu-Lung
collection PubMed
description Autism spectrum disorder (ASD) is characterized by cognitive inflexibility and social deficits. Probiotics have been demonstrated to play a promising role in managing the severity of ASD. However, there are no effective probiotics for clinical use. Identifying new probiotic strains for ameliorating ASD is therefore essential. Using the maternal immune activation (MIA)-based offspring ASD-like mouse model, a probiotic-based intervention strategy was examined in female mice. The gut commensal microbe Parabacteroides goldsteinii MTS01, which was previously demonstrated to exert multiple beneficial effects on chronic inflammation-related-diseases, was evaluated. Prenatal lipopolysaccharide (LPS) exposure induced leaky gut-related inflammatory phenotypes in the colon, increased LPS activity in sera, and induced autistic-like behaviors in offspring mice. By contrast, P. goldsteinii MTS01 treatment significantly reduced intestinal and systemic inflammation and ameliorated disease development. Transcriptomic analyses of MIA offspring indicated that in the intestine, P. goldsteinii MTS01 enhanced neuropeptide-related signaling and suppressed aberrant cell proliferation and inflammatory responses. In the hippocampus, P. goldsteinii MTS01 increased ribosomal/mitochondrial and antioxidant activities and decreased glutamate receptor signaling. Together, significant ameliorative effects of P. goldsteinii MTS01 on ASD relevant behaviors in MIA offspring were identified. Therefore, P. goldsteinii MTS01 could be developed as a next-generation probiotic for ameliorating ASD.
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spelling pubmed-96579482022-11-15 Amelioration of Maternal Immune Activation-Induced Autism Relevant Behaviors by Gut Commensal Parabacteroides goldsteinii Lin, Tzu-Lung Lu, Cha-Chen Chen, Ting-Wen Huang, Chih-Wei Lu, Jang-Jih Lai, Wei-Fan Wu, Ting-Shu Lai, Chih-Ho Lai, Hsin-Chih Chen, Ya-Lei Int J Mol Sci Article Autism spectrum disorder (ASD) is characterized by cognitive inflexibility and social deficits. Probiotics have been demonstrated to play a promising role in managing the severity of ASD. However, there are no effective probiotics for clinical use. Identifying new probiotic strains for ameliorating ASD is therefore essential. Using the maternal immune activation (MIA)-based offspring ASD-like mouse model, a probiotic-based intervention strategy was examined in female mice. The gut commensal microbe Parabacteroides goldsteinii MTS01, which was previously demonstrated to exert multiple beneficial effects on chronic inflammation-related-diseases, was evaluated. Prenatal lipopolysaccharide (LPS) exposure induced leaky gut-related inflammatory phenotypes in the colon, increased LPS activity in sera, and induced autistic-like behaviors in offspring mice. By contrast, P. goldsteinii MTS01 treatment significantly reduced intestinal and systemic inflammation and ameliorated disease development. Transcriptomic analyses of MIA offspring indicated that in the intestine, P. goldsteinii MTS01 enhanced neuropeptide-related signaling and suppressed aberrant cell proliferation and inflammatory responses. In the hippocampus, P. goldsteinii MTS01 increased ribosomal/mitochondrial and antioxidant activities and decreased glutamate receptor signaling. Together, significant ameliorative effects of P. goldsteinii MTS01 on ASD relevant behaviors in MIA offspring were identified. Therefore, P. goldsteinii MTS01 could be developed as a next-generation probiotic for ameliorating ASD. MDPI 2022-10-28 /pmc/articles/PMC9657948/ /pubmed/36361859 http://dx.doi.org/10.3390/ijms232113070 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Lin, Tzu-Lung
Lu, Cha-Chen
Chen, Ting-Wen
Huang, Chih-Wei
Lu, Jang-Jih
Lai, Wei-Fan
Wu, Ting-Shu
Lai, Chih-Ho
Lai, Hsin-Chih
Chen, Ya-Lei
Amelioration of Maternal Immune Activation-Induced Autism Relevant Behaviors by Gut Commensal Parabacteroides goldsteinii
title Amelioration of Maternal Immune Activation-Induced Autism Relevant Behaviors by Gut Commensal Parabacteroides goldsteinii
title_full Amelioration of Maternal Immune Activation-Induced Autism Relevant Behaviors by Gut Commensal Parabacteroides goldsteinii
title_fullStr Amelioration of Maternal Immune Activation-Induced Autism Relevant Behaviors by Gut Commensal Parabacteroides goldsteinii
title_full_unstemmed Amelioration of Maternal Immune Activation-Induced Autism Relevant Behaviors by Gut Commensal Parabacteroides goldsteinii
title_short Amelioration of Maternal Immune Activation-Induced Autism Relevant Behaviors by Gut Commensal Parabacteroides goldsteinii
title_sort amelioration of maternal immune activation-induced autism relevant behaviors by gut commensal parabacteroides goldsteinii
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9657948/
https://www.ncbi.nlm.nih.gov/pubmed/36361859
http://dx.doi.org/10.3390/ijms232113070
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