Pathogenic mechanism of intestinal microbiota involved in Guillain-Barre syndrome and with Bifidobacterium intervention

Abstract

IntroductionGuillain-barre syndrome (GBS) is an acute immune-mediated polyneuropathy, involving the peripheral nervous system. The pathogenicity of GBS lies on Th17/Treg imbalance which may be affected by intestinal microbiota. From the previous study, treatment with Bifidobacterium infantis (B. infantis) significantly improved the symptoms of experimental autoimmune neuritis (EAN) through reducing the levels of IL-17A. In the present study, we aimed to further investigate the pathogenic mechanisms of intestinal microbiota involved in GBS, with the intervention of Bifidobacterium.Material and methodsLewis rats (n = 18) were injected with P253-78 peptide and completed Freund's adjuvant to induce EAN model. The clinical scores, Hematoxylin–eosin (HE) staining and transmission electron microscopy at day 15 after immunization were used to determine the pathological changes. The levels of IL-17, IL-10 and TGF-β and the proportions of Th17 and Treg cells in lymphocytes of blood samples were used to decide the Th17 / Treg imbalance. The intestinal microbiota was detected using 16S rRNA technology, and the bacteria with significant changes were also detected in fecal specimens of GBS patients.ResultsB. infantis improved EAN, by decreasing clinical scores and pathological changes, thus improving Th17/Treg imbalance. Moreover, the number of Lactobacillus, Rumenococcus and Clostridium were significantly reduced whereas the number of Akkermansia, Escherichia and Coprococcus significantly increased in the EAN group, which was abrogated by B. infantis.ConclusionsImbalance of Th17/Tregs expression induced by imbalance of intestinal microbiota may get involved in GBS. However, B. infantis intervention can regulate Th17/Treg balance by regulating imbalanced intestinal microbiota, thus improving GBS.