Exploring Impact of Probiotic‐Fermented Soymilk on Dextran‐Sulfate‐Sodium‐Induced Ulcerative Colitis via Modulating Inflammation and Gut Microbiota Profile

Abstract

ScopeLactic acid bacteria with probiotic functions and their fermentation products play a role in regulating ulcerative colitis (UC). This study investigates the potential role of fermented soymilk (FSM4) rich in isoflavones on DSS‐induced UC.Methods and ResultsMice received 3% DSS and are supplemented daily once for 1 week by NFSM and FSM4. DSS usually causes intestinal inflammation and alters the gut microbiota. FSM4 intervention improves the UC‐related inflammation and gut microbiota alteration. It considerably decreases pro‐inflammatories such as TNF‐α, IL‐1β, and IL‐6 in serum and COX‐2 and MPO in colon tissues and pathogenic bacteria (Escherichia‐Shigella). This facilitates gut‐healthy bacteria growth. These healthy bacteria negatively correlat with pro‐inflammatory factors but positively associated with acetic acid, butyric acid, and propionic acid, which may act for PPAR‐γ pathway activating and NF‐κB p65 pathway inhibiting, lowering the risk of UC. Overall, FSM4 might alleviate UC and significantly reverse the dysbiosis of gut microbiota via the PPAR‐γ activation. It could be a good alternative for developing functional food to protect against UC.ConclusionFSM4 attenuates intestinal inflammation and modulates the SCFA‐producing bacteria growth, which enable the PPAR‐γ activation to alleviate the UC target, which could be a dietary intervention strategy for gut health.

Gut microbiota-mediated polyphenol metabolism is restrained by parasitic whipworm infection and associated with altered immune function in mice

“…Interestingly, we also found that the combination of PAC and T. muris infection led to the expansion of zOTUs corresponding to the Escherichia fergusonii which was absent in all other treatment groups ( p < 0.01 for interaction between diet and infection by two-way ANOVA; Figure 6c ). Given that the expansion of the Escherichia genus in the mouse GM is often indicative of a dysbiotic GM, 44 our data suggest that the intake of PAC together with SSD may be a risk factor for T. muris –induced dysbiosis compared to SSD consumption alone. Of note, this is consistent with some of our immunological data (e.g.…”

Promising probiotic-fermented soymilk for alleviating acute diarrhea: insights into the microbiome and metabolomics

“…16–18 This is consistent with our previous research, where FSM4 reduces intestinal inflammation and regulates the growth of SCFA-producing bacteria, allowing PPAR-γ activation to weaken UC stimulants. 35…”

Intestinal Fibrogenesis in Inflammatory Bowel Diseases: Exploring the Potential Role of Gut Microbiota Metabolites as Modulators

“…These effects are often mediated through the modulation of regulatory factors like PPAR-γ, ultimately reducing the activity of the TGF-β/Smad pathway [ 105 , 111 , 124 , 125 , 136 , 147 ]. In the gut, the mechanisms remain elusive but the most consolidated evidence suggests that SCFA-producing bacteria and LAB collaborate in anti-fibrotic mechanisms through the induction of PPAR-γ [ 132 , 133 , 140 ]. Specifically, SCFA-producing bacteria can induce PPAR-γ, while LAB create a microenvironment conducive to the growth of the SCFA-producing bacteria.…”

“…At the intestinal level, the oral administration of L. gasseri appears to have beneficial effects on the mucosa as it stimulates the release of IgA from DCs through the activation of TGF-β [ 139 ]. The administration of fermented soymilk to a preclinical model of DSS-induced colitis showed that LAB enhanced the growth of SCFA-producing bacteria, with an increase in PPAR-γ and a subsequent reduction in the inflammatory cytokines [ 140 ]. Although there are few studies analyzing the relationship between LA and pro-fibrotic patterns at the intestinal level, we speculate that LA may protect the gut from acute inflammatory responses in part by up-regulating anti-inflammatory pathways such as TGF-β, and in part by decreasing the fibrosis mediated by this cytokine.…”