Intestinal Mucosal Barrier Improvement with Prebiotics: Histological Evaluation of Longish Glucomannan Hydrolysates-Induced Innate T Lymphocyte Activities in Mice

Abstract

Use of prebiotics is a growing topic in healthcare. A lightweight molecule and water-soluble fiber ingredient, longish glucomannan hydrolysates (LGH), has been developed to improve the intestinal mucosal barrier and confer gut health benefits. This study aims to investigate the implications of continuous LGH intervening in intestinal epithelium integrity and protective immunity against chemical dextran sodium sulfate (DSS)-induced colitis. Twelve male BALB/c mice were randomly arranged into four groups. The LGH/DSS group had results in bodyweight variance, epithelial cell density, and aberrancy score as good as the LGH group, and both were equivalent to the control group. LGH consumption effectively protects the distal intestinal epithelium by activating innate T lymphocytes. Meanwhile, T-cell subsets in subepithelial interspersion take a bystander role in these microenvironmental alterations. Under this stress, the cluster of differentiation 3 (CD3)+ T cells infiltrate the epithelium, while CD4+ T cells inversely appear in submucosal large lymphoid aggregates/isolated lymphoid follicles (ILFs) in which significant CD3+, CD4+, and CD8+ T-cell populations agglomerate. Moreover, forkhead box P3 (Foxp3) and interleukin 17 (IL-17) are observed in these ILFs. Agglomerated CD4+ T-cell lineages may have roles with proinflammatory T helper 17 cells and anti-inflammatory regulatory T cells in balancing responses to intraluminal antigens. Collectively, LGH administration may function in immune modulation to protect against DSS-induced inflammation.

Inflammatory bowel disease therapeutic strategies by modulation of the microbiota: how and when to introduce pre-, pro-, syn-, or postbiotics?

“…To this day, colitis prevention studies have been mainly performed in adult murine models, and while they show for the most part, protective effects (53,(76)(77)(78), two studies described how inulin supplementation potentiated the severity of colitis (63,79). Recently, in line with our work, one study analyzed the effect of maternal intake of inulin on colitis development in rats, and described how it exacerbated intestinal damage and inflammation induced by DSS (80).…”

Maternal prebiotic supplementation impacts colitis development in offspring mice

“…Indeed, if colitis is not massively increased (no significant changes of the survival curves, the weight loss or the intestinal transit at day 18, the micro-DAI, the Lcn-2 faecal concentration or the global gene expression) the P + DSS group showed some exacerbated responses to DSS (transient changes in weight loss and transit time, an increase in DAI and faecal humidity) via modification of the distal colonic luminal microbiota composition and changes in distal colonic lipid content. To date, colitis prevention studies have mainly been performed in adult murine models, and while they showed, for the most part, protective effects (55)(56)(57)(58), two studies described how inulin supplementation potentiated the severity of colitis (59,60). Recently, in line with our work, one study analysed the effect of maternal intake of inulin on colitis development in rats and described how it exacerbated DSS-induced intestinal damage and inflammation (61).…”