Oral Administration of Probiotic Enterococcus durans to Ameliorate Experimental Autoimmune Encephalomyelitis in Mice

Introduction: Probiotics, including lactobacilli, have immunomodulatory activities with promising effects on inflammatory diseases. In this study, we evaluate the effect of Enterococcus durans (Edu) and three various Strains of lactobacilli (Lacto-mix), including L. rhamnosus, L. easel, and L. plantarum, to prevent Experimental Autoimmune Encephalomyelitis (EAE) features Methods: C57BL/6 female mice were inoculated with Myelin Oigodendrocyte Glycoprotein (MOG(35-55)) in CFA (complete Freund's adjuvant) to induce EAE. Five groups (n=6 in each group) of animals received saline or probiotics by oral gavage with 200 mu L of lactobacilli (1.5 x 10(8) CFU/mL) for 2 weeks before the immunization and during the test for one month. Results: Histopathological Studies showed an increase in infiltration of inflammatory cells and destruction of the myelin membrane in the EAE group but a decrease in inflammatory cells in the probiotic-treated animals. Pro-inflammatory cytokines (Interleukin [IL]-17 and Interferon [IFN]-gamma) concentration in the supernatant of the brain and spinal cord tissues showed a significant increase in the EAE compared with the normal saline group (P<0.01). While in the spinal cord tissue, there was a decrease in IL-17 in those animals treated with the Lactomix and Edu + Lacto-mix (P<0.01) and a significant decrease in IFN-gamma in those animals that received Edu (P<0.05). Western blot analysis of matrix metalloproteinase-9 and myelin basic protein showed a decrease and increase in treatment and EAE groups, respectively, compared to the normal control group. Conclusion: Our data suggest that probiotic Enterococcus durans and Lacto-mix prevents EAE, but further Studies are needed to clarify the exact mechanisms and their application in preclinical and clinical trials.

Automated summary

The study suggests that probiotics such as Enterococcus durans and lactobacilli can prevent the occurrence of Experimental Autoimmune Encephalomyelitis (EAE) by reducing inflammatory cell infiltration and decreasing the concentration of pro-inflammatory cytokines.