Gut relief formula attenuates dextran sulfate sodium-induced colitis by regulating NF-κB signaling and the intestinal microbiota in mice

2021 ◽  
Author(s):  
Xuemeng Si ◽  
Ning Liu ◽  
Hai Jia ◽  
Jiaqi Wang ◽  
Lina Pan ◽  
...  
Keyword(s):  
Intestinal Microbiota ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Mucosal Barrier ◽  
Mucosal Inflammation ◽  
Barrier Dysfunction

Gut relief formula administration alleviated mucosal inflammation and mucosal barrier dysfunction by inhibiting STAT3 and NF-κB activity and upregulating abundances of Lactobacillus in DSS-induced colitis.

Ingestion of Low Dose Pyroglutamyl Leucine Improves Dextran Sulfate Sodium-Induced Colitis and Intestinal Microbiota in Mice

2013 ◽  
Vol 61 (37) ◽  
pp. 8807-8813 ◽  
Author(s):  
Sayori Wada ◽  
Kenji Sato ◽  
Ryoko Ohta ◽  
Eri Wada ◽  
Yukiho Bou ◽  
...  
Keyword(s):  
Intestinal Microbiota ◽  
Low Dose ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium

scholarly journals SLC26A3 (DRA) prevents TNF-alpha-induced barrier dysfunction and dextran sulfate sodium-induced acute colitis

2018 ◽  
Vol 98 (4) ◽  
pp. 462-476 ◽  
Author(s):  
Xiangming Ding ◽  
Dongxiao Li ◽  
Mengke Li ◽  
Han Wang ◽  
Qin He ◽  
...  
Keyword(s):  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Tnf Alpha ◽  
Barrier Dysfunction ◽  
Acute Colitis

scholarly journals P288 Gut barrier failure biomarkers in IBD: Is there anything new beyond „The Wall’?

2020 ◽  
Vol 14 (Supplement_1) ◽  
pp. S296-S296
Author(s):  
N Sipeki ◽  
P Kovats ◽  
B Balogh ◽  
Z Shums ◽  
G L Norman ◽  
...  
Keyword(s):  
Cox Regression ◽  
Mucosal Damage ◽  
Mucosal Barrier ◽  
Mucosal Inflammation ◽  
Enzyme Linked Immunosorbent Assay ◽  
Disease Course ◽  
Barrier Dysfunction ◽  
Gut Barrier ◽  
Fatty Acid Binding ◽  
Cox Regression Analysis

Abstract Background Several defects in the many specialised components of mucosal barrier have been reported in inflammatory bowel disease (IBD). These alterations may represent a primary dysfunction in Crohn’s disease(CD), but they may also perpetuate chronic mucosal inflammation in ulcerative colitis(UC). Changes in intestinal permeability can predict IBD course. Methods We aim to determine the predictive potential of a panel of serological markers that reflect either mechanical or immunological gut barrier dysfunction regarding determination of disease phenotype, therapeutic strategy and long-term disease course in a prospective referral adult IBD patient cohort. Sera of 266 CD (m/f:112/154, median age:25 years, B1:80.1%, P1:18.0%) and 187 UC (m/f:86/101, median age:33 years, extensive colitis:28.3%) patients were assayed for intestinal fatty acid-binding protein(I-FABP) and various immunoglobulin A (IgA) molecules, anti-F-actin[AAA IgA/IgG] and anti-gliadin[AGA IgA/IgG]) by enzyme-linked immunosorbent assay (ELISA) along with 155 healthy controls (HCONT). Clinical data were available on unfavourable disease outcome as well as disease activity and medical treatment during the prospective follow-up (median: 143 and 135 mths for CD and UC respectively). Results In UC, median I-FABP level was significantly lower than in HCONT(177.2 vs. 244.3 pg/ml; p < 0.05). sIgA level was higher in both CD and UC compared with HCONT(51.2 and 46.0 vs. 29.2 μg/ml; p < 0.0001). AAA positivity with IgA type predominance was significantly higher in CD(40.2vs UC:15.7; HCONT:6.2%). AGA was also more prevalent in CD(16.5vs UC:6.7; HCONT:7.2%). There was an association between the presence of IgA type AAA or AGA and antimicrobial antibodies. ACA IgA was also more prevalent in case of AAA IgA positivity(52.9 vs. 32.7%, p = 0.009). PS/PT IgA positivity was higher in AGA IgA positive patients (33.3 vs. 7.6%, p = 0.001). Complicated disease behaviour at sample procurement was associated with the presence of AAA and AGA IgA positivity. In Kaplan–Meier analysis concomitant presence of IgA and IgG type AAA was associated with a shorter time to resective surgery (HR[95% CI]: 2.03[1.06–3.90]) along with a higher risk of a second surgery needed (HR[95% CI]: 2.82[1.14–6.98]). Sensitivity analysis showed that the later remained significant in B1 patients (p = 0.002) and also remained independent predictor in multivariate Cox-regression analysis comprising relevant clinical factors(HR[95% CI]: 2.88[1.07–7.78], p = 0.037). Conclusion The presence of AAA and AGA reflects the ongoing mucosal damage in IBD rather than has a value in predicting the disease course.

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

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Yingdi Zhang ◽  
Xiaojing Zhao ◽  
Yunjuan Zhu ◽  
Jingjing Ma ◽  
Haiqin Ma ◽  
...  
Keyword(s):  
Tight Junction ◽  
Peripheral Blood ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Intestinal Inflammation ◽  
Experimental Colitis ◽  
Mucosal Barrier ◽  
Intestinal Damage ◽  
Protective Effects ◽  
Junction Protein

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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