Complex dietary polysaccharide modulates gut immune function and microbiota, and promotes protection from autoimmune diabetes. Issue 1 (7th March 2019) - Gudi, Radhika
Summary: The dietary supplement and prebiotic values of β ‐glucan‐rich products have been widely recognized and dietary approaches for modulating autoimmunity have been increasingly explored, we assess the impact of oral administration of high‐purity yeast β ‐glucan (YBG) on gut immune function, microbiota and type 1 diabetes (T1D) using mouse models. Oral administration of this non‐digestible complex polysaccharide caused a dectin‐1‐dependent immune response involving increased expression of interleukin‐10 (IL‐10), retinaldehyde dehydrogenase (Raldh) and pro‐inflammatory cytokines in the gut mucosa. YBG‐exposed intestinal dendritic cells induced/expanded primarily Foxp3 +, IL‐10 + and IL‐17 + T cells, ex vivo . Importantly, prolonged oral administration of low‐dose YBG at pre‐diabetic stage suppressed insulitis and significantly delayed the appearance of T1D in non‐obese diabetic (NOD) mice. Further, prolonged treatment with YBG showed increased Foxp3 + T‐cell frequencies, and a significant change in the gut microbiota, particularly an increase in the abundance of Bacteroidetes and a decrease in the Firmicute members. Oral administration of YBG, together with Raldh‐substrate and β ‐cell antigen, resulted in better protection of NOD mice from T1D. These observations suggest that YBG not only has a prebiotic property, but also an oral tolerogenic‐adjuvant‐like effect, and these features could be exploited for modulating autoimmunity in T1D. Abstract : Considering the dietary supplement and prebiotic values of β ‐glucan‐rich products, this study determined the impact of oral administration of high‐purity yeast β ‐glucan (YBG) on gut immune function, microbiota and type 1 diabetes (T1D) using non‐obese diabetic (NOD) mice. Oral treatment with YBG caused increased Foxp3 + T‐cell frequencies, and a significant change in the gut microbiota, particularly an increase in the abundance of Bacteroidetes and a decrease in the Firmicute members, and suppression of insulitis and delay in the appearance of T1D in NOD mice. Further, oral administration of YBG, together with retinaldehyde dehydrogenase substrate and β ‐cell antigen, resulted in a better protection of NOD mice from T1D, suggesting that YBG not only has a prebiotic property, but also can produce an oral tolerogenic‐adjuvant‐like effect.