MedicalResearch.com Interview with:
Kouichi Ito, PhD
Department of Neurology
Robert Wood Johnson Medical School
MedicalResearch.com: What is the background for this study? What are the main findings?
Response: Multiple Sclerosis (MS) is an autoimmune disease of the central nervous system (CNS), and breakdown of immune tolerance to CNS proteins has been suggested to initiate CNS autoimmunity. Although the mechanism underlying the breakdown of immune tolerance to CNS proteins is still unknown, gut microbiota has been suggested to be involved in disease initiation and progression.
To investigate the etiology of Multiple Sclerosis, we have created humanized transgenic mice expressing MHC class II and T cell receptor genes isolated from an Multiple Sclerosis patient and showed that gut dysbiosis, alteration in intestinal microbial composition, can induce gut leakiness and subsequently trigger the development of neurological deficits through activation of complement C3 and reduction of CBLB and Foxp3 genes.
This study suggests that gut dysbiosis is one of the possible etiological factors for Multiple Sclerosis.
MedicalResearch.com: What should clinicians and patients take away from your report?
Response: Translocation of intestinal microbial components into the bloodstream caused by dysbiosis-induced leaky gut can increase the risk of autoimmune diseases including Multiple Sclerosis. Therefore, it is important to maintain healthy gut flora to prevent the development of Multiple Sclerosis.
MedicalResearch.com: What recommendations do you have for future research as a result of this study?
Response: It could be important to investigate the intestinal microbial products involved in the development of Multiple Sclerosis and how to prevent their translocation into the bloodstream.
MedicalResearch.com: Thank you for your contribution to the MedicalResearch.com community.
Gut dysbiosis breaks immunological tolerance toward the central nervous system during young adulthood PNAS 2017 114 (44) E9318-E9327; published ahead of print October 16, 2017, doi:10.1073/pnas.1615715114
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