scholarly journals A murine colitis model developed using a combination of dextran sulfate sodium and Citrobacter rodentium

2018 ◽  
Vol 56 (4) ◽  
pp. 272-279
Author(s):  
Jin-Il Park ◽  
Sun-Min Seo ◽  
Jong-Hyung Park ◽  
Hee-Yeon Jeon ◽  
Jun-Young Kim ◽  
...  
Keyword(s):  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Citrobacter Rodentium ◽  
Murine Colitis ◽  
Colitis Model

scholarly journals Erratum to: A murine colitis model developed using a combination of dextran sulfate sodium and Citrobacter rodentium

2018 ◽  
Vol 56 (5) ◽  
pp. 372-372
Author(s):  
Jin-Il Park ◽  
Sun-Min Seo ◽  
Jong-Hyung Park ◽  
Hee-Yeon Jeon ◽  
Jun-Young Kim ◽  
...  
Keyword(s):  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Citrobacter Rodentium ◽  
Murine Colitis ◽  
Colitis Model

scholarly journals Molecular and Microbial Signatures Predictive of Prebiotic Action of Neoagarotetraose in a Dextran Sulfate Sodium-Induced Murine Colitis Model

2020 ◽  
Vol 8 (7) ◽  
pp. 995
Author(s):  
Fang Liu ◽  
Jianan Liu ◽  
Thomas T.Y. Wang ◽  
Zhen Liu ◽  
Changhu Xue ◽  
...  
Keyword(s):  
Gut Microbiome ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Intestinal Inflammation ◽  
16S Rrna Gene Sequencing ◽  
Rrna Gene ◽  
Murine Colitis ◽  
Bioactive Properties ◽  
Rrna Gene Sequencing ◽  
Colitis Model

Neoagarotetraose (NT), a hydrolytic product of agar by β-agarase, is known to possess bioactive properties. However, the mechanisms via which NT alleviates intestinal inflammation remain unknown. In this study, a dextran sulfate sodium (DSS)-induced murine model was developed to evaluate the effect of NT on gut microbiome and microbial metabolism using 16S rRNA gene sequencing and untargeted metabolomics. Our data demonstrate that NT ingestion improved gut integrity and inflammation scores. NT reversed the abundance of Proteobacteria from an elevated level induced by DSS and significantly increased the abundance of Verrucomicrobia. Further, NT significantly increased the abundance of Akkermansia and Lactobacillus and concomitantly decreased that of Sutterella, which were among the important features identified by random forests analysis contributing to classification accuracy for NT supplementation. A microbial signature consisting of Adlercreutzia (denominator) and Turicibacter (numerator) predicted the NT supplementation status. Moreover, NT significantly modulated multiple gut metabolites, particularly those related to histidine, polyamine and tocopherol metabolism. Together, our findings provided novel insights into the mechanisms by which NT modulated the gut microbiome and metabolome and should facilitate the development of NT as a potent prebiotic for colitis management.

The ameliorative effect of a Lactobacillus strain with good adhesion ability against dextran sulfate sodium-induced murine colitis

2019 ◽  
Vol 10 (1) ◽  
pp. 397-409 ◽  
Author(s):  
Guangqiang Wang ◽  
Yingnan Liu ◽  
Zhi Lu ◽  
Yiting Yang ◽  
Yongjun Xia ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Good Adhesion ◽  
Disease Symptoms ◽  
Murine Colitis ◽  
Adhesion Ability ◽  
Ameliorative Effect ◽  
Excellent Adhesion ◽  
Colitis Model

The objective of this study was to effectively screen out a Lactobacillus strain with excellent adhesion ability and ameliorative effect on the disease symptoms of a murine ulcerative colitis model.

Malvidin 3‐Glucoside Modulated Gut Microbial Dysbiosis and Global Metabolome Disrupted in a Murine Colitis Model Induced by Dextran Sulfate Sodium

2019 ◽  
Vol 63 (21) ◽  
pp. 1900455 ◽  
Author(s):  
Fang Liu ◽  
Thomas T. Y. Wang ◽  
Qingjuan Tang ◽  
Changhu Xue ◽  
Robert W. Li ◽  
...  
Keyword(s):  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Murine Colitis ◽  
Microbial Dysbiosis ◽  
Colitis Model

scholarly journals P031 Class A1 scavenger receptor mediates macrophage polarization and apoptotic progression in a murine dextran sulfate sodium-induced colitis

2021 ◽  
Vol 15 (Supplement_1) ◽  
pp. S146-S147
Author(s):  
J Su ◽  
C Xie ◽  
Y Hu ◽  
Q Huang ◽  
H Shi ◽  
...  
Keyword(s):  
Treatment Group ◽  
Signaling Pathway ◽  
Colonic Mucosa ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Scavenger Receptor ◽  
Negative Regulator ◽  
Antibody Treatment ◽  
Murine Colitis ◽  
Colitis Model

Abstract Background This study aimed to investigate the role of class A1 scavenger receptor (SR-A1) for regulating macrophage function and apoptotic pathway during intestinal inflammation of inflammatory bowel disease (IBD) in a DSS-induced murine colitis model. Methods A murine colitis model was established by feeding with 5% dextran sulfate sodium (DSS). Treatment groups were injected intravenously with SR-A1 antibody (100ug/kg), and control groups were injected with the vehicle only. Inflammatory activity and histological changes were evaluated on Day 8, and the percentage of macrophage markers in lamina propria mononuclear cells (LPMC) was measured by flow cytometer. The apoptosis and proliferation of intestinal epithelial cells were detected by TUNEL and Ki67 staining, and the expressions of related signaling pathway protein were determined with western blot. Results Treatment group showed a preventive effect on colitis symptoms and fewer inflammatory cell infiltrates compared with control group. After SR-A1 antibody treatment, flow cytometry of LPMC indicated that the percentage of F4/80+CD206+ Macrophages was elevated, while the percentage of F4/80+CD11c+ Macrophages was not obviously changed. Immunohistochemistry revealed that TUNEL-positive cells were significantly downregulated and Ki67- positive cells were upregulated in colonic mucosa of treatment group. In addition, the expressions of TLR4, MyD88 and NF-kB proteins in colonic mucosa were decreased after SR-A1 antibody injection. Conclusion Treatment with SR-A1 antibody could ameliorate macrophage-associated inflammatory response and epithelial cell apoptosis in a murine colitis model, which suggested that SR-A1 was a negative regulator of M2 polarization in IBD. SR-A1 mediated its effect by synergizing with TLR4/ MyD88 / NF-kB signaling pathway. Our research identified SR-A1 as a potential therapeutic target in IBD.

scholarly journals Acetylcholine-producing T cells augment innate immune-driven colitis but are redundant in T cell-driven colitis

2019 ◽  
Vol 317 (5) ◽  
pp. G557-G568 ◽  
Author(s):  
Rose A. Willemze ◽  
David J. Brinkman ◽  
Olaf Welting ◽  
Patricia H. P. van Hamersveld ◽  
Caroline Verseijden ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Nerve Stimulation ◽  
Vagus Nerve Stimulation ◽  
Inflammatory Cytokine ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Innate Immune ◽  
Cytokine Levels ◽  
Colitis Model

Clinical trials suggest that vagus nerve stimulation presents an alternative approach to classical immune suppression in Crohn's disease. T cells capable of producing acetylcholine (ChAT+ T cells) in the spleen are essential mediators of the anti-inflammatory effect of vagus nerve stimulation. Besides the spleen, ChAT+ T cells are found abundantly in Peyer’s patches of the small intestine. However, the role of ChAT+ T cells in colitis pathogenesis is unknown. Here, we made use of CD4creChATfl/fl mice (CD4ChAT−/− mice) lacking ChAT expression specifically in CD4+ T cells. Littermates (ChATfl/fl mice) served as controls. In acute dextran sulfate sodium (DSS)-induced colitis (7 days of 2% DSS in drinking water), CD4ChAT−/− mice showed attenuated colitis and lower intestinal inflammatory cytokine levels compared with ChATfl/fl mice. In contrast, in a resolution model of DSS-induced colitis (5 days of 2% DSS followed by 7 days without DSS), CD4ChAT−/− mice demonstrated a worsened colitis recovery and augmented colonic histological inflammation scores and inflammatory cytokine levels as compared with ChATfl/fl mice. In a transfer colitis model using CD4+CD45RBhigh T cells, T cells from CD4ChAT−/− mice induced a similar level of colitis compared with ChATfl/fl T cells. Together, our results indicate that ChAT+ T cells aggravate the acute innate immune response upon mucosal barrier disruption in an acute DSS-induced colitis model, whereas they are supporting the later resolution process of this innate immune-driven colitis. Surprisingly, ChAT expression in T cells seems redundant in the context of T cell-driven colitis. NEW & NOTEWORTHY By using different mouse models of experimental colitis, we provide evidence that in dextran sulfate sodium-induced colitis, ChAT+ T cells capable of producing acetylcholine worsen the acute immune response, whereas they support the later healing phase of this innate immune-driven colitis.

Sign in / Sign up

Export Citation Format

Share Document