Probiotic Mixture Protects Dextran Sulfate Sodium-Induced Colitis by Altering Tight Junction Protein Expressions and Increasing Tregs

Bifico is a probiotic mixture containing Bifidobacterium, Lactobacillus acidophilus, and Enterococcus. Studies support that Bifico has a protective effect in experimental colitis (IL-10-deficient and TNBS) models and in patients with inflammatory bowel disease (IBD). However, the mechanism underlying the protective effects of this mixture of probiotic bacteria remains incompletely clear. Here, we investigated the effect of Bifico on intestinal inflammation. In an in vivo experiment, dextran sulfate sodium was used to induce colitis. Bifico treatment significantly attenuated the severity of colitis in this model. Bifico increased the expression of tight junction proteins (TJs). In addition, Bifico increased the number of Tregs, but reduced the number of total CD4+ T cells in the peripheral blood. Furthermore, the expression of colonic CD4 protein was decreased while the level of forkhead box P3 (Foxp3) was upregulated. These results suggested that Bifico exerts beneficial effects on experimental colitis by increasing the expressions of TJs, upregulating the number of Tregs, and reducing the total CD4+ T cell number in both colon and peripheral blood. The intestinal damage in the pretreated + treated-Bifico-colitis group was more severe than that in only the pretreated-Bifico-colitis group. This suggested that Bifico might aggravate intestinal damage when the mucosal barrier is impaired.

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Protective Effects of Japanese Black Vinegar “Kurozu” and Its Sediment “Kurozu Moromimatsu” on Dextran Sulfate Sodium-induced Experimental Colitis

Colitis ◽

10.5772/25698 ◽

2012 ◽

Author(s):

Toru Shizuma ◽

Chiharu Tanaka ◽

Hidezo Mori ◽

Naoto Fukuyam

Keyword(s):

Dextran Sulfate ◽

Dextran Sulfate Sodium ◽

Experimental Colitis ◽

Protective Effects

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Intervention withα-Ketoglutarate Ameliorates Colitis-Related Colorectal Carcinoma via Modulation of the Gut Microbiome

BioMed Research International ◽

10.1155/2019/8020785 ◽

2019 ◽

Vol 2019 ◽

pp. 1-9 ◽

Cited By ~ 4

Author(s):

Si Li ◽

Chenxing Fu ◽

Yurong Zhao ◽

Jianhua He

Keyword(s):

Dextran Sulfate ◽

Dextran Sulfate Sodium ◽

Intestinal Inflammation ◽

Intestinal Microbiome ◽

Protective Effects ◽

Opportunistic Pathogens ◽

Immunomodulatory Effects ◽

Chronic Intestinal Inflammation ◽

Antitumour Effects ◽

Necrosis Factor

The intestinal microbiome plays a crucial role in promoting intestinal health, and perturbations to its constitution may result in chronic intestinal inflammation and lead to colorectal cancer (CRC).α-Ketoglutarate is an important intermediary in the NF-κB-mediated inflammatory pathway that maintains intestinal homeostasis and prevents initiation of intestinal inflammation, a known precursor to carcinoma development. The objective of this study was to assess the potential protective effects ofα-ketoglutarate intervention against CRC development, which may arise due to its known anti-inflammatory and antitumour effects. CRC was induced in C57BL/6 mice using azoxymethane (AOM) and dextran sulfate sodium (DSS). Tumour frequency, histological rating, and colonic microbiota were assessed in colonic samples. The findings demonstrated thatα-ketoglutarate offered significant protection against CRC development in mice. Furthermore,α-ketoglutarate also exhibited immunomodulatory effects mediated via downregulation of interleukin (IL)-6, IL-22, tumour necrosis factor (TNF)-α, and IL-1βcytokines. Finally, intervention withα-ketoglutarate tended to minimise the frequency of opportunistic pathogens (EscherichiaandEnterococcus) while increasing the populations ofAkkermansia, Butyricicoccus,Clostridium,andRuminococcus. Taken together, our findings show that dietaryα-ketoglutarate intervention may protect against inflammation-related CRC.

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Protective Effects of Kurozu and Kurozu Moromimatsu on Dextran Sulfate Sodium-Induced Experimental Colitis

Digestive Diseases and Sciences ◽

10.1007/s10620-010-1432-x ◽

2010 ◽

Vol 56 (5) ◽

pp. 1387-1392 ◽

Cited By ~ 4

Author(s):

Toru Shizuma ◽

Kazuo Ishiwata ◽

Masanobu Nagano ◽

Hidezo Mori ◽

Naoto Fukuyama

Keyword(s):

Dextran Sulfate ◽

Dextran Sulfate Sodium ◽

Experimental Colitis ◽

Protective Effects

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Formononetin Administration Ameliorates Dextran Sulfate Sodium-Induced Acute Colitis by Inhibiting NLRP3 Inflammasome Signaling Pathway

Mediators of Inflammation ◽

10.1155/2018/3048532 ◽

2018 ◽

Vol 2018 ◽

pp. 1-12 ◽

Cited By ~ 12

Author(s):

Dacheng Wu ◽

Keyan Wu ◽

Qingtian Zhu ◽

Weiming Xiao ◽

Qing Shan ◽

...

Keyword(s):

Tight Junction ◽

Nlrp3 Inflammasome ◽

Dextran Sulfate ◽

Dextran Sulfate Sodium ◽

Acute Injury ◽

Dependent Manner ◽

Protective Effects ◽

Tight Junction Proteins ◽

Acute Colitis ◽

Junction Proteins

Formononetin is a kind of isoflavone compound and has been reported to possess anti-inflammatory properties. In this present study, we aimed to explore the protective effects of formononetin on dextran sulfate sodium- (DSS-) induced acute colitis. By intraperitoneal injection of formononetin in mice, the disease severity of colitis was attenuated in a dose-dependent manner, mainly manifesting as relieved clinical symptoms of colitis, mitigated colonic epithelial cell injury, and upregulations of colonic tight junction proteins levels (ZO-1, claudin-1, and occludin). Meanwhile, our study found that formononetin significantly prevented acute injury of colonic cells induced by TNF-α in vitro, specifically manifesting as the increased expressions of colonic tight junction proteins (ZO-1, claudin-1, and occludin). In addition, the result showed that formononetin could reduce the NLRP3 pathway protein levels (NLRP3, ASC, IL-1β) in vivo and vitro, and MCC950, the NLRP3 specific inhibitor, could alleviate the DSS-induced mice acute colitis. Furthermore, in the foundation of administrating MCC950 to inhibit activation of NLRP3 inflammasome, we failed to observe the protective effects of formononetin on acute colitis in mice. Collectively, our study for the first time confirmed the protective effects of formononetin on DSS-induced acute colitis via inhibiting the NLRP3 inflammasome pathway activation.

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Loss of the Tight Junction Protein ZO-1 in Dextran Sulfate Sodium Induced Colitis

Journal of Surgical Research ◽

10.1016/j.jss.2006.07.050 ◽

2007 ◽

Vol 140 (1) ◽

pp. 12-19 ◽

Cited By ~ 197

Author(s):

Lisa S. Poritz ◽

Kristian I. Garver ◽

Cecelia Green ◽

Leo Fitzpatrick ◽

Francesca Ruggiero ◽

...

Keyword(s):

Tight Junction ◽

Dextran Sulfate ◽

Dextran Sulfate Sodium ◽

Tight Junction Protein ◽

Junction Protein

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Curcumin Regulated the Homeostasis of Memory T Cell and Ameliorated Dextran Sulfate Sodium-Induced Experimental Colitis

Frontiers in Pharmacology ◽

10.3389/fphar.2020.630244 ◽

2021 ◽

Vol 11 ◽

Author(s):

You-Bao Zhong ◽

Zeng-Ping Kang ◽

Bu-Gao Zhou ◽

Hai-Yan Wang ◽

Jian Long ◽

...

Keyword(s):

Inflammatory Bowel Disease ◽

Bowel Disease ◽

Peripheral Blood ◽

Dextran Sulfate ◽

Dextran Sulfate Sodium ◽

Experimental Colitis ◽

Immune Memory ◽

Effector Memory ◽

Colon Tissue ◽

Inflammatory Bowel

Immune memory is protective against reinvasion by pathogens in the homeostatic state, while immune memory disorders can cause autoimmune disease, including inflammatory bowel disease. Curcumin is a natural compound shown to be effective against human inflammatory bowel disease and experimental colitis, but the underlying mechanism is unclear. Here, experimental colitis was induced by dextran sulfate sodium (DSS) in this study. Significant changes in the percentages of naïve, central memory T (TCM), and effector memory (TEM) cells and their CD4+ and CD8+ subsets were found in the peripheral blood of mice with colitis using flow cytometry. After 7 days of continuous curcumin (100 mg/kg/day) administration, the DSS-induced experimental colitis was effectively relieved, with significant decreases in the ratio of day weight to initial body weight, colonic weight, pathological injury score, levels of proinflammatory cytokines IL-7, IL-15, and IL-21, colonic mucosal ulceration, and amount of inflammatory infiltrate. Importantly, curcumin significantly restored the percentages of naïve, TCM, and TEM cells and their CD4+ and CD8+ subpopulations. In addition, curcumin significantly inhibited the activation of the JAK1/STAT5 signaling pathway, downregulation of JAK1, STAT5, and p-STAT5 proteins in colon tissue, and upregulation of PIAS1 proteins. These results suggested that curcumin effectively regulated the differentiation of naïve, TCM, and TEM cells in the peripheral blood to alleviate DSS-induced experimental colitis, which might be related to the inhibition of JAK1/STAT5 signaling activity.

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A Role of Exopolysaccharide Produced by Streptococcus thermophilus in the Intestinal Inflammation and Mucosal Barrier in Caco-2 Monolayer and Dextran Sulphate Sodium-Induced Experimental Murine Colitis

Molecules ◽

10.3390/molecules24030513 ◽

2019 ◽

Vol 24 (3) ◽

pp. 513 ◽

Cited By ~ 12

Author(s):

Yun Chen ◽

Ming Zhang ◽

Fazheng Ren

Keyword(s):

Tight Junction ◽

Intestinal Inflammation ◽

Gastrointestinal Disease ◽

Streptococcus Thermophilus ◽

Water Soluble ◽

Mucosal Barrier ◽

Dextran Sulphate ◽

Dextran Sulphate Sodium ◽

Junction Protein ◽

Mucosal Barrier Function

Exopolysaccharide (EPS) produced by probiotics may play an important role in gastrointestinal disease prevention, including ulcerative colitis. However, there is no literature reporting on the intervention effects of purified EPS. The aim of this study was to investigate the alleviating effect of the purified EPS produced by Streptococcus thermophilus MN-BM-A01 on murine model of colitis induced by dextran sulphate sodium (DSS). A water-soluble heteropolysaccharide (EPS-1) isolated from MN-BM-A01 was composed of rhamnose, glucose, galactose, and mannose in a molar ratio of 12.9:26.0:60.9:0.25, with molecular weight of 4.23 × 105 Da. After EPS-1 administration, the disease severity of mouse colitis was significantly alleviated, mainly manifesting as the decrease of disease activity index and mitigated colonic epithelial cell injury. Meanwhile, pro-inflammatory cytokines levels (tumor necrosis factor-α, interleukin-6, and interferon-γ) were significantly suppressed, the reduced expressions of tight junction protein (claudin-1, occludin, and E-canherin) were counteracted. In addition, the results in vitro showed that EPS-1 protected intestinal barrier integrity from the disruption by lipopolysaccharide in Caco-2 monolayer, increased expression of tight junction and alleviated pro-inflammatory response. Collectively, our study confirmed the protective effects of purified EPS produced by Streptococcus thermophilus on acute colitis via alleviating intestinal inflammation and improving mucosal barrier function.

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Exopolysaccharide Produced by Lactiplantibacillus plantarum-12 Alleviates Intestinal Inflammation and Colon Cancer Symptoms by Modulating the Gut Microbiome and Metabolites of C57BL/6 Mice Treated by Azoxymethane/Dextran Sulfate Sodium Salt

Foods ◽

10.3390/foods10123060 ◽

2021 ◽

Vol 10 (12) ◽

pp. 3060

Author(s):

Fenglian Ma ◽

Yinglong Song ◽

Mengying Sun ◽

Arong Wang ◽

Shujuan Jiang ◽

...

Keyword(s):

Colon Cancer ◽

Oral Administration ◽

Sodium Salt ◽

Dextran Sulfate ◽

Dextran Sulfate Sodium ◽

Intestinal Inflammation ◽

Inflammatory Factors ◽

Inflammatory Factor ◽

Cancer Symptoms ◽

Junction Protein

Exopolysaccharide produced by Lactiplantibacillus plantarum-12 (LPEPS) exhibited the anti-proliferating effect on human colon cancer cell line HT-29 in vitro. The purpose of the study was to determine the alleviating effects of LPEPS on colon cancer development of the C57BL/6 mice treated by azoxymethane/dextran sulfate sodium salt (AOM/DSS). The C57BL/6 mice treated by AOM/DSS were orally administered LPEPS daily for 85 days. The results showed that LPEPS oral administration enhanced colon tight-junction protein expression and ameliorated colon shortening and tumor burden of the AOM/DSS treated mice. Furthermore, LPEPS oral administration significantly reduced pro-inflammatory factors TNF-α, IL-8, and IL-1β levels and increased anti-inflammatory factor IL-10 level in the serum of the AOM/DSS-treated mice. LPEPS oral administration reversed the alterations of gut flora in AOM/DSS-treated mice, as evidenced by the increasing of the abundance of Bacteroidetes, Bacteroidetes/Firmicutes ratio, Muribaculaceae, Burkholderiaceae, and norank_o__Rhodospirillales and the decreasing of the abundance of Firmicutes, Desulfovibrionaceae, Erysipelotrichaceae, and Helicobacteraceae. The fecal metabolites of the AOM/DSS-treated mice were altered by LPEPS oral administration, involving lipid metabolism and amino acid metabolism. Together, these results suggested that LPEPS oral administration alleviated AOM/DSS-induced colon cancer symptoms of the C57BL/6 mice by modulating gut microbiota and metabolites, enhancing intestine barrier, inhibiting NF-κB pathway, and activating caspase cascade.

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