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Helicobacter pylori infection reduces disease severity in an experimental model of multiple sclerosis

      Background: Infection with Helicobacter pylori may reduce the risk of developing inflammatory diseases. The infection is also less common amongst patients with multiple sclerosis (MS), an inflammatory demyelinating disease of the central nervous system. However, there is no direct evidence that H. pylori is protective.
      Objective: We aimed to investigate the impact of H. pylori infection on experimental autoimmune encephalomyelitis (EAE), an animal model for MS.
      Design/methods: Groups of C57BL/6 mice were infected with H. pylori, or given the diluent alone as a placebo, prior to induction of EAE with myelin oligodendrocyte glycoprotein (MOG) peptide in CFA. Clinical scores were assessed and at termination of the experiment, tissues were harvested. CD4+ T-cell subsets were quantified by flow cytometry, and T-cell proliferation assays were performed.
      Results: H. pylori infection significantly reduced the severity of EAE clinical scores and the proliferation of MOG peptide-specific T-cells in infected mice. There was a 4-fold reduction in the frequency of CD4+ cells in the CNS. CD4+ populations in both the CNS and the spleens of infected mice also contained greatly reduced proportions of IFNγ+, IL-17+, T-bet+, and RORγt + cells. The frequencies of Foxp3+ cells were equivalent. There were no differences in the frequency of splenic CD4+ cells expressing markers of apoptosis between infected and uninfected animals.
      Conclusions: H. pylori infection exerted some protection against EAE in mice, inhibiting both Th1 and Th17 responses. We provide experimental evidence to suggest that H. pylori may provide protection against immune-mediated diseases such as MS.