Literature DB >> 29908492

Treatment of Guillain-Barré syndrome with Bifidobacterium infantis through regulation of T helper cells subsets.

Peng Shi1, Hongdang Qu2, Di Nian3, Yuhua Chen1, Xiaolin Liu1, Qiang Li1, Qianqian Li1, Chun Wang1, Ming Ye1, Bo Ma1.   

Abstract

BACKGROUND: Guillain-Barré syndrome (GBS) is a rare, autoimmune-mediated disease. The use of Bifidobacterium is reportedly effective in alleviating GBS since they act by regulating T helper (Th) cells.
OBJECTIVES: In this study, we explored the differentiation of T helper cell subsets in patients with GBS. We also evaluated the effect of GBS on Bifidobacterium levels in patients and the likely protective influence of this bacterium in alleviating the disease in an animal model.
MATERIALS AND METHODS: We used flow cytometry, and real-time polymerase chain reaction (PCR) to determine the T cell subsets differentiation among 30 GBS patients and 20 healthy controls (HC). The concentration of Bifidobacterium was assayed by real-time PCR. Experimental autoimmune neuritis (EAN) animal model was established to support the protective role of Bifidobacterium in GBS.
RESULTS: The expression of Th cells, Th2 and Th17 in the patients was significantly higher than that in the HC, while Treg cells decreased substantially. Moreover, the levels of Bifidobacterium in the GBS patients were considerably lower than those in the HC, the concentration of Bifidobacterium correlating with Th2 and Th17 subsets negatively. Treatment with Bifidobacterium significantly reduced the levels of Th2 and Th17 and promoted the levels of Treg cells.
CONCLUSIONS: We concluded from this study that Bifidobacterium alleviated GBS by regulating Th cells, although in-depth studies might be required to fully understand the mechanism of action.
Copyright © 2018 The Authors. Published by Elsevier B.V. All rights reserved.

Entities:  

Keywords:  Bifidobacterium; CD4(+)T lymphocyte; Experimental autoimmune neuritis; Guillain-Barré syndrome

Mesh:

Year:  2018        PMID: 29908492     DOI: 10.1016/j.intimp.2018.06.015

Source DB:  PubMed          Journal:  Int Immunopharmacol        ISSN: 1567-5769            Impact factor:   4.932


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