scholarly journals Innovative Animal Model of DSS-Induced Ulcerative Colitis in Pseudo Germ-Free Mice

Cells ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 2571
Author(s):  
Sona Gancarcikova ◽  
Stanislav Lauko ◽  
Gabriela Hrckova ◽  
Zuzana Andrejcakova ◽  
Vanda Hajduckova ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Animal Model ◽  
Cellular Proliferation ◽  
Sodium Sulphate ◽  
Mucosal Barrier ◽  
Pathogenic Microorganisms ◽  
Dextran Sodium Sulphate ◽  
Germ Free ◽  
Proliferation And Apoptosis ◽  
Selective Antibiotics

The aim of this study was to investigate the use of a standardized animal model subjected to antibiotic treatment, and the effects of this treatment on the course of dextran sodium sulphate (DSS)-induced colitis in mice. By decontamination with selective antibiotics and observation of pathogenesis of ulcerative colitis (UC) induced chemically by exposure of mice to various concentrations of DSS, we obtained an optimum animal PGF model of acute UC manifested by mucin depletion, epithelial degeneration and necrosis, leading to the disappearance of epithelial cells, infiltration of lamina propria and submucosa with neutrophils, cryptitis, and accompanied by decreased viability of intestinal microbiota, loss of body weight, dehydration, moderate rectal bleeding, and a decrease in the selected markers of cellular proliferation and apoptosis. The obtained PGF model did not exhibit changes that could contribute to inflammation by means of alteration of the metabolic status and the induced dysbiosis did not serve as a bearer of pathogenic microorganisms participating in development of ulcerative colitis. The inflammatory process was induced particularly by exposure to DSS and its toxic action on compactness and integrity of mucosal barrier in the large intestine. This offers new possibilities of the use of this animal model in studies with or without participation of pathogenic microbiota in IBD pathogenesis.

scholarly journals The New Salicylate Derivative UR-1505 Modulates the Th2/Humoral Response in a Dextran Sodium Sulphate Model of Colitis That Resembles Ulcerative Colitis

2009 ◽  
Vol 109 (2) ◽  
pp. 315-318 ◽  
Author(s):  
Elvira Bailón ◽  
Juan Román ◽  
Isabel Ramis ◽  
Pedro Michelena ◽  
Dolors Balsa ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Humoral Response ◽  
Sodium Sulphate ◽  
Dextran Sodium Sulphate

scholarly journals A Molecular Targeted Immunotherapeutic Strategy for Ulcerative Colitis via Dual-targeting Nanoparticles Delivering miR-146b to Intestinal Macrophages

2018 ◽  
Vol 13 (4) ◽  
pp. 482-494 ◽  
Author(s):  
Feihong Deng ◽  
Shuying He ◽  
Shudan Cui ◽  
Yanqiang Shi ◽  
Yuyong Tan ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Oral Delivery ◽  
Macrophage Activation ◽  
Mucosal Damage ◽  
Sodium Sulphate ◽  
Mucosal Barrier ◽  
Mucosal Regeneration ◽  
M1 Macrophage ◽  
Mucosal Barrier Function ◽  
Immunotherapeutic Strategy

Abstract Background and Aims Macrophages are a promising therapeutic target for intestinal mucosal repair. MiR-146b appears to control macrophage activation and cell proliferation. Methods By loading miR-146b mimic on mannose-modified trimethyl chitosan [MTC]-conjugated nanoparticles [NPs] [MTC-miR146b], a molecular targeted immunotherapeutic approach was developed to selectively target intestinal macrophages for mucosal regeneration and tumourigenesis in mouse models. Results We first confirmed that miR-146b expression was significantly enhanced during mucosal regeneration in a murine colitis model. Moreover， after mucosal damage, MTC-miR146b mimic-treated wild-type mice had dramatically restored body weight and mucosal barrier function compared with MTC-NC treated mice. Strikingly, MTC-miR146b mimic oral administration protected miR-146b-deficient mice from dextran sodium sulphate [DSS] injury and the colitis-associated cancer process. Mechanistically, miR-146b strongly inhibited M1 macrophage activation by suppressing the Toll-like receptor 4 [TLR4] signalling pathway, resulting in the repression of the induction of pro-inflammatory cytokines including TNF-α, IL-6, and IL-1β. More importantly, miR-146b overexpression in bone marrow-derived macrophages [BMDMs] in M1 differentiation conditions induced a phenotype similar to M2 macrophages and improved the proliferation of co-cultured colonic epithelial cells via STAT3-dependent IL-10 production. Conclusions MTC-miR146b should be regarded as an effective candidate for oral delivery and could improve the efficacy of immunotherapies for ulcerative colitis and colitis-associated cancer.

scholarly journals Titanium Dioxide Presents a Different Profile in Dextran Sodium Sulphate-Induced Experimental Colitis in Mice Lacking the IBD Risk Gene Ptpn2 in Myeloid Cells

2021 ◽  
Vol 22 (2) ◽  
pp. 772
Author(s):  
Javier Conde ◽  
Marlene Schwarzfischer ◽  
Egle Katkeviciute ◽  
Janine Häfliger ◽  
Anna Niechcial ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Titanium Dioxide ◽  
Genetic Risk ◽  
Intestinal Inflammation ◽  
Sodium Sulphate ◽  
Food Additive ◽  
Wild Type ◽  
Dextran Sodium Sulphate ◽  
Risk Gene ◽  
The Impact

Environmental and genetic factors have been demonstrated to contribute to the development of inflammatory bowel disease (IBD). Recent studies suggested that the food additive; titanium dioxide (TiO2) might play a causative role in the disease. Therefore, in the present study we aimed to explore the interaction between the food additive TiO2 and the well-characterized IBD risk gene protein tyrosine phosphatase non-receptor type 2 (Ptpn2) and their role in the development of intestinal inflammation. Dextran sodium sulphate (DSS)-induced acute colitis was performed in mice lacking the expression of Ptpn2 in myeloid cells (Ptpn2LysMCre) or their wild type littermates (Ptpn2fl/fl) and exposed to the microparticle TiO2. The impact of Ptpn2 on TiO2 signalling pathways and TiO2-induced IL-1β and IL-10 levels were studied using bone marrow-derived macrophages (BMDMs). Ptpn2LysMCre exposed to TiO2 exhibited more severe intestinal inflammation than their wild type counterparts. This effect was likely due to the impact of TiO2 on the differentiation of intestinal macrophages, suppressing the number of anti-inflammatory macrophages in Ptpn2 deficient mice. Moreover, we also found that TiO2 was able to induce the secretion of IL-1β via mitogen-activated proteins kinases (MAPKs) and to repress the expression of IL-10 in bone marrow-derived macrophages via MAPK-independent pathways. This is the first evidence of the cooperation between the genetic risk factor Ptpn2 and the environmental factor TiO2 in the regulation of intestinal inflammation. The results presented here suggest that the ingestion of certain industrial compounds should be taken into account, especially in individuals with increased genetic risk

scholarly journals Orally administered RDP58 reduces the severity of dextran sodium sulphate induced colitis

2002 ◽  
Vol 61 (Supplement 2) ◽  
pp. 19ii-24 ◽  
Author(s):  
R Boismenu ◽  
Y Chen ◽  
K Chou ◽  
A El-Sheikh ◽  
R Buelow
Keyword(s):  
Sodium Sulphate ◽  
Dextran Sodium Sulphate

scholarly journals Ablation of ceramide synthase 2 exacerbates dextran sodium sulphate-induced colitis in mice due to increased intestinal permeability

2017 ◽  
Vol 21 (12) ◽  
pp. 3565-3578 ◽  
Author(s):  
Ye-Ryung Kim ◽  
Giora Volpert ◽  
Kyong-Oh Shin ◽  
So-Yeon Kim ◽  
Sun-Hye Shin ◽  
...  
Keyword(s):  
Intestinal Permeability ◽  
Sodium Sulphate ◽  
Ceramide Synthase ◽  
Dextran Sodium Sulphate
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