Microbiology: Alterations of the gut microbiota in multiple sclerosis

Alterations in the gut microbiota correlate with changes in the expression of immune defence genes in patients suffering from multiple sclerosis (MS), finds a study published in Nature Communications. Further studies are needed to determine whether these changes could be used as potential biomarkers for assessing disease progression in the future.

Gut bacteria are known to have an influence on the function of the immune system, with changes in the abundances of gut microorganisms correlating with the development of autoimmune disorders. A previous study of 20 patients suffering from MS and 40 healthy controls found microbiota alterations in the patients with MS, but the potential connection between microbiota, therapy and changes in immunity has not been previously examined.

Howard Weiner and colleagues sampled and analysed the gut microbiota of 60 patients with MS and 43 healthy controls. They found that microorganisms such as Methanobrevibacter (the main methane-producing microbe in the human gut) were more abundant in patients than in controls. These changes correlated with variations in the expression of immune response genes in blood immune cells (for instance, genes involved in cell maturation and signalling pathways). They also showed that, in the patients, other microbiota alterations correlated with the use of immunosuppressive medication. In addition, within a smaller cohort of patients, elevated levels of methane were found in the breath of patients compared to controls, which is consistent with increased abundance of Methanobrevibacter in MS patients.

Further research with larger cohorts of patients and samples collected during disease progression is needed to test whether these alterations in microbiota may play a role in, or are a consequence of, changes in immune gene expression or the disease itself. Future work will also help determine whether the observed alterations in the microbiota or in methane in the breath could be used as disease biomarkers.

doi: 10.1038/ncomms12015

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