Beneficial changes in the gut microbiome of patients with multiple sclerosis after consumption of Neu-REFIX B-glucan in a clinical trial

Background Multiple sclerosis (MS) is a debilitating demyelinating disease and recent evidences are giving cues towards correlation of disease severity to gut microbiome dysbiosis. However, there haven’t been any reported interventions that beneficially modifies the gut microbiome to yield a clinically discernible improvement. Having earlier reported the clinical effects of a biological response modifier beta-glucan (BRMG) produced by the N-163 strain of Aureobasidum pullulans , commercially available as Neu-REFIX, which decreased the biomarkers of inflammation and produced beneficial immune-modulation in twelve MS patients in 60 days, we evaluated their gut microbiome in the present study. Methods Twelve patients diagnosed with MS participated in the study. Each consumed 16 g gel of the NEU-REFIX beta-Glucan for 60 days. Whole genome metagenomic sequencing was performed on the fecal samples before and after Neu-REFIX intervention. Results Post-intervention analysis showed that Actinobacteria followed by Bacteroides was the major family. Abundance of beneficial genera such as Bifidobacterium, Collinsela, Prevotella, Lactobacillus and species such as Prevotella copri (p-value=0.4), Bifidobacterium longum (p-value=0.2), Faecalibacterium prausnitzii (p-value=0.06), Siphoviridae (p-value=0.06) increased while inflammation associated genera such as Blautia (p-value=0.06) , Ruminococcus (p-value=0.007) and Dorea (p-value = 0.03) decreased in abundance. Conclusion Restoration of gut eubiosis in terms of both increase in abundance of the good microbiome and suppression of the harmful ones which also correlate with earlier reported clinical improvement in MS patients makes this Neu-REFIX beta-glucan, a potential disease modifying therapy (DMT) requiring larger studies for validation in MS and other auto-immune-inflammatory conditions where a safe intervention for immune modulation is vital.