Min Cui

Bio: Min Cui is an academic researcher from First Affiliated Hospital of Xinjiang Medical University. The author has contributed to research in topics: Colitis & Red meat. The author has co-authored 1 publications.

High Red Meat Intake Exacerbates Dextran Sulfate-Induced Colitis by Altering Gut Microbiota in Mice.

Abstract: Inflammatory bowel disease (IBD) is a serious hazard to public health, but the precise etiology of the disease is unclear. High intake of red meat diet is closely related to the occurrence of IBD. In this study, we investigated whether the high intake of red meat can increase the sensitivity of colitis and the underlying mechanism. Mice were fed with different levels of red meat for 8 weeks and then the colonic contents were analyzed by 16S rRNA sequencing. Then 3% dextran sulfate sodium was used to induce colitis in mice. We observed the severity of colitis and inflammatory cytokines. We found that high-dose red meat caused intestinal microbiota disorder, reduced the relative abundance of Lachnospiraceae_NK4A136_group, Faecalibaculum, Blautia and Dubosiella, and increased the relative abundance of Bacteroides and Alistipes. This in turn leads to an increase in colitis and inflammatory cytokine secretion. Moreover, we found that high red meat intake impaired the colon barrier integrity and decreased the expression of ZO-1, claudin, and occludin. We also found high red meat intake induced the production of more inflammatory cytokines such as IL-1β, TNF-α, IL-17, and IL-6 and inflammatory inducible enzymes such as COX-2 and iNOS in dextran sulfate sodium-induced colitis. These results suggest that we should optimize the diet and reduce the intake of red meat to prevent the occurrence of IBD.

Dietary Patterns and Gut Microbiota Changes in Inflammatory Bowel Disease: Current Insights and Future Challenges

Abstract: Inflammatory bowel disease (IBD) is a result of a complex interplay between genes, host immune response, gut microbiota, and environmental factors. As one of the crucial environmental factors, diet plays a pivotal role in the modulation of gut microbiota community and the development of IBD. In this review, we present an overview of dietary patterns involved in the pathogenesis and management of IBD, and analyze the associated gut microbial alterations. A Westernized diet rich in protein, fats and refined carbohydrates tends to cause dysbiosis and promote IBD progression. Some dietary patterns have been found effective in obtaining IBD clinical remission, including Crohn’s Disease Exclusion Diet (CDED), Mediterranean diet (MD), Anti-Inflammatory Diet (AID), the low-“Fermentable Oligo-, Di-, Mono-saccharides and Polyols” (FODMAP) diet, Specific Carbohydrate Diet (SCD), and plant-based diet, etc. Overall, many researchers have reported the role of diet in regulating gut microbiota and the IBD disease course. However, more prospective studies are required to achieve consistent and solid conclusions in the future. This review provides some recommendations for studies exploring novel and potential dietary strategies that prevent IBD.

Linarin ameliorates dextran sulfate sodium-induced colitis in C57BL/6J mice via the improvement of intestinal barrier, suppression of inflammatory responses and modulation of gut microbiota.

Abstract: Linarin is a natural flavonoid compound found in Chrysanthemum indicum, Mentha species and other plants with various biological activities. The study aimed to investigate the protective effect of linarin supplementation on dextran sulfate sodium (DSS)-induced colitis in C57BL/6J mice and its potential mechanisms. The results showed that doses of linarin at 25 and 50 mg kg-1 day-1 alleviated the DSS-induced histopathological damage, and improved the mucosal layer and intestinal barrier function. Importantly, Linarin significantly suppressed the levels of myeloperoxidase activity and pro-inflammatory cytokines (IL-6, TNF-α, IFN-γ and IL-1β) in the colon, and enhanced the mRNA level of anti-inflammatory cytokine (IL-10). Moreover, 50 mg kg-1 day-1 linarin reversed the gut microbiota damaged by DSS, including Alistipes, Rikenella and Clostridia UCG-014_norank. Linarin also partly increased the relative abundance of short-chain fatty acids (SCFAs)-producing bacteria, including Lactobacillus, Roseburia, Parabacteroides and Blautia, and elevated the contents of SCFAs. Collectively, linarin attenuates DSS-induced colitis in mice, suggesting that linarin may be a promising nutritional strategy for reducing inflammatory bowel disease.

Effects of Different Ionic Polysaccharides in Cooked Lean Pork Batters on Intestinal Health in Mice

Abstract: The effects of cooked lean pork batters with three ionic types of polysaccharides (anionic xanthan-gum/sodium-alginate, neutral curdlan-gum/konjac-gum and cationic chitosan) on the intestinal health of mice were investigated in this study. The results showed that the zeta potential in the sodium-alginate group (−31.35 mV) was higher (p < 0.05) than that in the chitosan group (−26.00 mV), thus promoting the protein hydrolysis in the anionic group because of electrostatic repulsion. The content of total free amino acids in the small intestine in the xanthan-gum and sodium-alginate groups (2754.68 μg and 2733.72 μg, respectively) were higher (p < 0.05) than that in the chitosan group (1949.78 μg), which could decrease the amount of undigested protein entering the colon. The two anionic groups could also increase the abundance of Lactobacillus and the balance of Faecalibaculum and Alistipes in the colon. The content of proinflammatory factor IL−6 of colon tissues in the sodium-alginate group (1.02 ng/mL) was lower (p < 0.05) than that in chitosan, curdlan-gum and konjac-gum groups (1.29, 1.31 and 1.31 ng/mL, respectively). The result of haematoxylin-eosin staining of the colon also revealed that sodium alginate was beneficial for colonic health. The two neutral groups increased the content of faecal short-chain fatty acids in mice. These results demonstrated that anionic polysaccharides have potential for developing functional low-fat meat products.

Colonic Epithelial Circadian Disruption Worsens Dextran Sulfate Sodium–Induced Colitis

Abstract: Abstract Background Disruption of central circadian rhythms likely mediated by changes in microbiota and a decrease in gut-derived metabolites like short chain fatty acids (SCFAs) negatively impacts colonic barrier homeostasis. We aimed to explore the effects of isolated peripheral colonic circadian disruption on the colonic barrier in a mouse model of colitis and explore the mechanisms, including intestinal microbiota community structure and function. Methods Colon epithelial cell circadian rhythms were conditionally genetically disrupted in mice: TS4Cre-BMAL1lox (cBMAL1KO) with TS4Cre as control animals. Colitis was induced through 5 days of 2% dextran sulfate sodium (DSS). Disease activity index and intestinal barrier were assessed, as were fecal microbiota and metabolites. Results Colitis symptoms were worse in mice with peripheral circadian disruption (cBMAL1KO). Specifically, the disease activity index and intestinal permeability were significantly higher in circadian-disrupted mice compared with control animals (TS4Cre) (P < .05). The worsening of colitis appears to be mediated, in part, through JAK (Janus kinase)-mediated STAT3 (signal transducer and activator of transcription 3), which was significantly elevated in circadian-disrupted (cBMAL1KO) mice treated with DSS (P < .05). Circadian-disrupted (cBMAL1KO) mice also had decreased SCFA metabolite concentrations and decreased relative abundances of SCFA-producing bacteria in their stool when compared with control animals (TS4Cre). Conclusions Disruption of intestinal circadian rhythms in colonic epithelial cells promoted more severe colitis, increased inflammatory mediators (STAT3 [signal transducer and activator of transcription 3]), and decreased gut microbiota–derived SCFAs compared with DSS alone. Further investigation elucidating the molecular mechanisms behind these findings could provide novel circadian directed targets and strategies in the treatment of inflammatory bowel disease.

A westernized diet changed the colonic bacterial composition and metabolite concentration in a dextran sulfate sodium pig model for ulcerative colitis

Abstract: Introduction Ulcerative colitis (UC) is characterized by chronic inflammation in the colonic epithelium and has a blurred etiology. A western diet and microbial dysbiosis in the colon were reported to play a role in UC development. In this study, we investigated the effect of a westernized diet, i.e., increasing fat and protein content by including ground beef, on the colonic bacterial composition in a dextran sulfate sodium (DexSS) challenged pig study. Methods The experiment was carried out in three complete blocks following a 2×2 factorial design including 24 six-week old pigs, fed either a standard diet (CT) or the standard diet substituted with 15% ground beef to simulate a typical westernized diet (WD). Colitis was induced in half of the pigs on each dietary treatment by oral administration of DexSS (DSS and WD+DSS, respectively). Samples from proximal and distal colon and feces were collected. Results and discussion Bacterial alpha diversity was unaffected by experimental block, and sample type. In proximal colon, WD group had similar alpha diversity to CT group and the WD+DSS group showed the lowest alpha diversity compared to the other treatment groups. There was a significant interaction between western diet and DexSS for beta diversity, based on Bray-Curtis dissimilarly. The westernized diet and DexSS resulted in three and seven differentially abundant phyla, 21 and 65 species, respectively, mainly associated with the Firmicutes and Bacteroidota phyla followed by Spirochaetota, Desulfobacterota, and Proteobacteria. The concentration of short-chain fatty acids (SCFA) was lowest in the distal colon. Treatment had a slight effect on the estimates for microbial metabolites that might have valuable biological relevance for future studies. The concentration of putrescine in the colon and feces and that of total biogenic amines was highest in the WD+DSS group. We conclude that a westernized diet could be a potential risk factor and an exacerbating agent for UC by reducing the abundance of SCFA-producing bacteria, increasing the abundance of pathogens such as Helicobacter trogontum, and by increasing the concentration of microbial proteolytic-derived metabolites in the colon.