Pathogenic mechanism of intestinal microbiota involved in Guillain-Barré syndrome and with intervention.

INTRODUCTION

Guillain-Barré syndrome (GBS) is an acute immune-mediated polyneuropathy, involving the peripheral nervous system. The pathogenicity of GBS involves Th17/Treg imbalance, which may be affected by intestinal microbiota. From the previous study, treatment with () 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 .

MATERIAL AND METHODS

Lewis rats ( = 18) were injected with P2 peptide and complete Freund's adjuvant to induce the 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 transforming growth factor-β (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.

RESULTS

improved EAN, by decreasing clinical scores and pathological changes, thus improving Th17/Treg imbalance. Moreover, the number of and were significantly reduced whereas the number of and significantly increased in the EAN group, which was abrogated by .

CONCLUSIONS

Imbalance of Th17/Tregs expression induced by imbalance of intestinal microbiota may get involved in GBS. However, intervention can regulate Th17/Treg balance by regulating imbalanced intestinal microbiota, thus improving GBS.