Galactooligosaccharide Treatment Alleviates DSS-Induced Colonic Inflammation in Caco-2 Cell Model

Abstract

The biological activities of dietary bioactive polysaccharides have been largely explored. Studies on the immunomodulating effects of oligosaccharides and polysaccharides have shown that they are able to modulate innate immunity. Prebiotics are a class of poorly digested carbohydrates that are mainly produced from dietary fibers, which are carbohydrate polymers with ten or more monomeric units as defined by the Codex Alimentarius Commission in 2009. Considering the capacity of prebiotics in reducing gut inflammation, the aim of this study was to investigate the anti-inflammatory activity of galactooligosaccharide (Bimuno® GOS) in an in vitro model of ulcerative colitis (UC)-like inflamed intestinal cells. Differentiated Caco-2 cells were exposed to 2 % dextran-sulfate-sodium salt (DSS) to induce inflammation, and then with different concentrations of Bimuno GOS (1–1,000 μg/ml). Cell monolayer permeability, tight- and adherent junction protein distribution, pro-inflammatory cytokine secretion, and NF-kB cascade were assessed. Bimuno GOS at different concentrations, while not affecting cell monolayer permeability, was shown to counteract UC-like intestinal inflammatory responses and damages induced by DSS. Indeed, Bimuno GOS was able to counteract the detrimental effects of DSS on cell permeability, determined by transepithelial electrical resistance, phenol red apparent permeability, and tight- and adherent junction protein distribution. Furthermore, Bimuno GOS inhibited the DSS-induced NF-kB nuclear translocation and pro-inflammatory cytokine secretion. Further analyses showed that Bimuno GOS was able to revert the expression levels of most of the proteins involved in the NF-kB cascade to control levels. Thus, the prebiotic Bimuno GOS can be a safe and effective way to modulate the gut inflammatory state through NF-kB pathway modulation, and could possibly further improve efficacy in inducing remission of UC.

Dietary protocatechuic acid redistributes tight junction proteins by targeting Rho-associated protein kinase to improve intestinal barrier function

“…DSS administration can reportedly cause a decrease in the colon length because DSS causes redistribution of tight junctions, resulting in increased cell permeability, which in turn increases inflammatory cytokines, causing inflammation in the intestinal tissue, and destroying intestinal tissue cells. 28,46 In the DSS treatment groups, the colon lengths were significantly reduced, and PCA administration reversed this phenotype in a dose-dependently manner (Fig. 6B).…”

Maternal intervention with a combination of galacto-oligosaccharides and hyocholic acids during late gestation and lactation increased the reproductive performance, colostrum composition, antioxidant and altered intestinal microflora in sows

“…Nevertheless, the maternal will undergo metabolic syndrome during normal pregnancy, especially in late gestation, which decreases dramatically gut microbiota diversity and richness ( Collado et al, 2010 ; Cheng et al, 2018 ). Recent studies showed that GOS had the promising potential to alleviate metabolic diseases by regulating the intestinal flora ( Silk et al, 2009 ; Roselli et al, 2022 ). The dominating prebiotic functions of GOS are to selectively stimulate probiotic proliferation ( Bifidobacteria , Bacteroides ) and to produce short-chain fatty acids by fermenting ( Li et al, 2015 ; Vulevic et al, 2015 ; Grimaldi et al, 2016 ).…”

P62/SQSTM1 binds with claudin-2 to target for selective autophagy in stressed intestinal epithelium

“…However, current study was undertaken to examine epithelial-intrinsic effects of claudin-2 expression under conditions of colitis/stress. Recent studies have used similar in vitro treatment of IECs by DSS to model colitis-induced epithelial injury 44 – 47 . However, both, DSS treatment and starvation resulted in a similar fate for claudin-2 and IECs survival, which suggest that the autophagy-mediated regulation of claudin-2 may not be limited to IBD.…”