4.8 Review

Targeting the gut to treat multiple sclerosis

Journal

JOURNAL OF CLINICAL INVESTIGATION
Volume 131, Issue 13, Pages -

Publisher

AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI143774

Keywords

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Funding

  1. National Institute of Neurological Disorders and Stroke/NIH [R01 NS102633-01]
  2. Office of the Assistant Secretary of Defense for Health Affairs, through the Multiple Sclerosis Research Pro-gram [W81XWH1410156]
  3. Leon and Harriet Felman Fund for Human MS Research
  4. Fondazione Italiana Sclerosi Multipla (FISM) [2014/R/15]
  5. Italian Multiple Sclerosis Society research fellowship [FISM 2018/B/1]
  6. National Multiple Sclerosis Society Post-Doctoral Fellowship [FG190734474]
  7. National MS Society Career Transition Fellowship [TA-1805-31003]
  8. Whitelaw Terry, Jr./Valerie Terry funds
  9. 5 per mille public funding
  10. U.S. Department of Defense (DOD) [W81XWH1410156] Funding Source: U.S. Department of Defense (DOD)

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The gut-brain axis refers to interactions between gut microbiota and nervous, immune, and endocrine systems, potentially playing a role in multiple sclerosis pathogenesis. Studies have shown that pwMS are more likely to exhibit altered microbiota and metabolites, with approaches such as antibiotics and fecal microbiota transplantation showing promising outcomes in preventing CNS inflammation. However, more research is needed to establish consistent results and large-scale randomized controlled trials are lacking in this area.
The gut-brain axis (GBA) refers to the complex interactions between the gut microbiota and the nervous, immune, and endocrine systems, together linking brain and gut functions. Perturbations of the GBA have been reported in people with multiple sclerosis (pwMS), suggesting a possible role in disease pathogenesis and making it a potential therapeutic target. While research in the area is still in its infancy, a number of studies revealed that pwMS are more likely to exhibit altered microbiota, altered levels of short chain fatty acids and secondary bile products, and increased intestinal permeability. However, specific microbes and metabolites identified across studies and cohorts vary greatly. Small clinical and preclinical trials in pwMS and mouse models, in which microbial composition was manipulated through the use of antibiotics, fecal microbiota transplantation, and probiotic supplements, have provided promising outcomes in preventing CNS inflammation. However, results are not always consistent, and large-scale randomized controlled trials are lacking. Herein, we give an overview of how the GBA could contribute to MS pathogenesis, examine the different approaches tested to modulate the GBA, and discuss how they may impact neuroinflammation and demyelination in the CNS.

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