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B.infantis enhances immunotherapy for Guillain-Barre syndrome through regulating PD-1

BACKGROUND: Guillain-Barré syndrome (GBS) is a rare, autoimmune disease. B.infantis is reported to be effective in alleviating GBS by regulating abnormal function of T helper (Th) cells. OBJECTIVES: In this study, T cells were isolated from healthy and GBS patients. The therapeutic effect of Bifidob...

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Autores principales: Shi, Peng, Nian, Di, Qu, Hongdang, Ye, Ming, Wang, Chun, Li, Li, Li, Qian
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9883859/
https://www.ncbi.nlm.nih.gov/pubmed/36709251
http://dx.doi.org/10.1186/s12883-022-03046-w
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author Shi, Peng
Nian, Di
Qu, Hongdang
Ye, Ming
Wang, Chun
Li, Li
Li, Qian
author_facet Shi, Peng
Nian, Di
Qu, Hongdang
Ye, Ming
Wang, Chun
Li, Li
Li, Qian
author_sort Shi, Peng
collection PubMed
description BACKGROUND: Guillain-Barré syndrome (GBS) is a rare, autoimmune disease. B.infantis is reported to be effective in alleviating GBS by regulating abnormal function of T helper (Th) cells. OBJECTIVES: In this study, T cells were isolated from healthy and GBS patients. The therapeutic effect of Bifidobacterium infantis (B.infantis) and whether it is achieved by PD-1 was examined at cellular and animal models. METHODS: We used CCK-8, flow cytometry and real-time PCR to determine the differentiation of T cell subsets at cellular level. Then, an experimental autoimmune neuritis (EAN) animal model using six-week SD rats (n = 30, male) weighing 180–200 g was established to support the role of B. infantis in GBS through PD-1. RESULTS: B. infantis inhibited the proliferation and promoted apoptosis of T cells from GBS. At the same time, the expression levels of PD-1 increased, which was correlated with decreased T-bet (Th1) and ROR-γt (Th17) and increased Foxp3 (Treg) expression. Moreover, B. infantis alleviated the symptoms of GBS. Th1 and Th17 cells decreased while Treg cells increased after B. infantis treatment, which could be partly abrogated by PD-1 inhibitor. CONCLUSIONS: We concluded from this study that B.infantis alleviated GBS partly through PD-1. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12883-022-03046-w.
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spelling pubmed-98838592023-01-29 B.infantis enhances immunotherapy for Guillain-Barre syndrome through regulating PD-1 Shi, Peng Nian, Di Qu, Hongdang Ye, Ming Wang, Chun Li, Li Li, Qian BMC Neurol Research BACKGROUND: Guillain-Barré syndrome (GBS) is a rare, autoimmune disease. B.infantis is reported to be effective in alleviating GBS by regulating abnormal function of T helper (Th) cells. OBJECTIVES: In this study, T cells were isolated from healthy and GBS patients. The therapeutic effect of Bifidobacterium infantis (B.infantis) and whether it is achieved by PD-1 was examined at cellular and animal models. METHODS: We used CCK-8, flow cytometry and real-time PCR to determine the differentiation of T cell subsets at cellular level. Then, an experimental autoimmune neuritis (EAN) animal model using six-week SD rats (n = 30, male) weighing 180–200 g was established to support the role of B. infantis in GBS through PD-1. RESULTS: B. infantis inhibited the proliferation and promoted apoptosis of T cells from GBS. At the same time, the expression levels of PD-1 increased, which was correlated with decreased T-bet (Th1) and ROR-γt (Th17) and increased Foxp3 (Treg) expression. Moreover, B. infantis alleviated the symptoms of GBS. Th1 and Th17 cells decreased while Treg cells increased after B. infantis treatment, which could be partly abrogated by PD-1 inhibitor. CONCLUSIONS: We concluded from this study that B.infantis alleviated GBS partly through PD-1. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12883-022-03046-w. BioMed Central 2023-01-28 /pmc/articles/PMC9883859/ /pubmed/36709251 http://dx.doi.org/10.1186/s12883-022-03046-w Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Research
Shi, Peng
Nian, Di
Qu, Hongdang
Ye, Ming
Wang, Chun
Li, Li
Li, Qian
B.infantis enhances immunotherapy for Guillain-Barre syndrome through regulating PD-1
title B.infantis enhances immunotherapy for Guillain-Barre syndrome through regulating PD-1
title_full B.infantis enhances immunotherapy for Guillain-Barre syndrome through regulating PD-1
title_fullStr B.infantis enhances immunotherapy for Guillain-Barre syndrome through regulating PD-1
title_full_unstemmed B.infantis enhances immunotherapy for Guillain-Barre syndrome through regulating PD-1
title_short B.infantis enhances immunotherapy for Guillain-Barre syndrome through regulating PD-1
title_sort b.infantis enhances immunotherapy for guillain-barre syndrome through regulating pd-1
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9883859/
https://www.ncbi.nlm.nih.gov/pubmed/36709251
http://dx.doi.org/10.1186/s12883-022-03046-w
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