Dietary Turmeric Consumption Alleviates Ulcerative Colitis via Restoring Tryptophan Metabolism and Alleviating Gut Microbiota Dysbiosis in Mice

Abstract

This study was designed to first verify the protective capacity of turmeric powder (TP) as a traditional cooking spice against dextran sulfate sodium (DSS)-induced intestinal inflammation and intestine microbiota imbalance. The DSS-induced mice were fed a standard rodent chow supplemented with or without TP (8%) for 37 days. The results indicated that the pathological phenotype, gut barrier disruption, and colon inflammation of DSS-induced mice were significantly improved through supplementation of TP. In addition, 16S rRNA-based microbiota or targeted metabolomics analysis indicated that TP ameliorated intestinal microbiota dysbiosis caused by DSS and particularly enhanced the abundances of probiotics correlated with tryptophan metabolism, such as Lactobacillus and Bifidobacterium, where the cecal tryptophan was metabolized to indole-3-propionic acid and indole-3-acetic acid. Consumption of TP markedly enhanced the expression levels of colonic aromatic hydrocarbon receptors and further increased the expressions of intestinal tight junction proteins and interleukin-22 in the colitis mice. Collectively, these findings manifest the protective actions of dietary TP consumption against ulcerative colitis via restoring the intestinal microbiota disorders, promoting microbial metabolism, and improving intestinal barrier damage.

Urolithin A Alleviates Colitis in Mice by Improving Gut Microbiota Dysbiosis, Modulating Microbial Tryptophan Metabolism, and Triggering AhR Activation

“…39 Recently, monomeric IL-22 treatment was reported to inhibit the production of pro-inflammatory cytokines and alleviate DSS-induced acute colitis in mice, 40 and increased serum content and enhanced colonic expression of IL-22 were widely found to be associated with improved colitis phenotypes. 3 Our results revealed that UroA treatment significantly increased serum IL-22 levels, as expected, and decreased the content of IL-10 in serum (Figures 3C and 6F), suggesting that the anticolitis activity of UroA was primarily related to IL-22 in this study.…”

“…Therefore, IL-10 is regarded as a blocker of pro-inflammatory responses in many colitis models in response to polysaccharide, polyphenol, and peptide treatments . However, in some other studies, serum IL-10 was increased in response to DSS treatment, suggesting an opposite indicator to show the severity of colitis in mice, indicating the more complex function of IL-10 in IBD; these findings explain the results that IBD patients display no significant benefit from treatment with recombinant IL-10 and PEGylated fusion proteins . In addition, the majority of IL-22-associated molecules are encoded by IBD susceptibility genes, indicating the vital role of IL-22 .…”

“…1 However, dietary changes in recent decades have led to maladaptive shifts in this integration, which are believed to be implicated in the rising incidence of inflammatory bowel disease (IBD) worldwide. 2 Ulcerative colitis and Crohn's disease are the main subtypes of IBD, leading to chronic inflammatory phenotypes of the gastrointestinal tract, characterized by weight loss, diarrhea, bloody stool, and inflammatory injury of the intestinal mucosa, 3 which have substantial effects on individuals' lives and increase health expenditure. The underlying etiology of IBD remains poorly elucidated due to the complex relationships between hereditary factors and environmental factors during IBD development, including genetic modification, host immune stress, mucosal barrier deficiency, and gut microbiota dysbiosis.…”

Colon-Targeted Release of Turmeric Nonextractable Polyphenols and Their Anticolitis Potential via Gut Microbiota-Dependent Alleviation on Intestinal Barrier Dysfunction in Mice

“…Animals were randomly divided into five groups ( n = 10): normal control group (NC), DSS group (DSS), DSS + EP group (EPs), DSS + NEP group (NEPs), and DSS + DF group (DFs). The mouse model of colitis was established by drinking water containing 1.5% DSS for four cycles (4 days/cycle, with a 7 day recovery). , The NC and DSS groups of C57/B6J mice were given a normal chow diet, whereas EP, NEP, and DF groups of mice received a normal chow diet supplemented with corresponding turmeric fractions, namely, EPs, NEPs, and DFs, respectively. EPs (crude extraction), NEPs (residue after EP extraction), and DFs (residue after extracting the bound polyphenols from NEPs) were added to the normal chow diet with 8% proportion, which was chosen based on our previous experiments .…”

“…The scores of body weight loss, stool hardness, and fecal blood were recorded according to our previously published studies. 27 Besides, hematoxylin and eosin (H&E) staining was used to study the damage of the colon tissues. The mouse colon tissue was fixed in 4% neutral formalin solution, embedded in paraffin, and sliced into 5−6 μm, and the slices were visualized under a light microscope (Carl Zeiss AG, Jena, Germany).…”