Alterations of the human gut microbiome in multiple sclerosis

Alterations of the human gut microbiome in multiple sclerosis

Received 6 Sep 2015 | Accepted 20 May 2016 | Published 28 Jun 2016 | Sushrut Jangi, Roopali Gandhi, Laura M. Cox, Ning Li, Felipe von Glehn, Raymond Yan, Bonny Patel, Maria Antonietta Mazzola, Shirong Liu, Bonnie L. Glanz, Sandra Cook, Stephanie Tankou, Fiona Stuart, Kirsy Melo, Parham Nejad, Kathleen Smith, Begüm D. Topçuolu, James Holden, Pia Kivisäkk, Tanuja Chitnis, Philip L. De Jager, Francisco J. Quintana, Georg K. Gerber, Lynn Bry & Howard L. Weiner
The gut microbiome plays a crucial role in immune function and has been implicated in various autoimmune disorders, including multiple sclerosis (MS). This study investigates the gut microbiome in MS patients (n=60) and healthy controls (n=43) using 16S rRNA sequencing. Key findings include increased *Methanobrevibacter* and *Akkermansia* and decreased *Butyricimonas* in MS patients, which correlate with variations in genes involved in dendritic cell maturation, interferon signaling, and NF-kB signaling pathways in circulating T cells and monocytes. Patients on disease-modifying treatment show increased *Prevotella* and *Sutterella* and decreased *Sarcina*. A second cohort of MS patients showed elevated breath methane, consistent with increased *Methanobrevibacter* in the gut. These alterations suggest that the gut microbiome may play a role in MS pathogenesis, potentially through immune modulation. Further research is needed to determine whether these microbial changes are a cause or consequence of MS.The gut microbiome plays a crucial role in immune function and has been implicated in various autoimmune disorders, including multiple sclerosis (MS). This study investigates the gut microbiome in MS patients (n=60) and healthy controls (n=43) using 16S rRNA sequencing. Key findings include increased *Methanobrevibacter* and *Akkermansia* and decreased *Butyricimonas* in MS patients, which correlate with variations in genes involved in dendritic cell maturation, interferon signaling, and NF-kB signaling pathways in circulating T cells and monocytes. Patients on disease-modifying treatment show increased *Prevotella* and *Sutterella* and decreased *Sarcina*. A second cohort of MS patients showed elevated breath methane, consistent with increased *Methanobrevibacter* in the gut. These alterations suggest that the gut microbiome may play a role in MS pathogenesis, potentially through immune modulation. Further research is needed to determine whether these microbial changes are a cause or consequence of MS.
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