Cargando…
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...
Autores principales: | , , , , , , |
---|---|
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 |
Sumario: | 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. |
---|