scholarly journals Impaired Resolution of Inflammation in theEndoglinHeterozygous Mouse Model of Chronic Colitis

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
Madonna R. Peter ◽  
Mirjana Jerkic ◽  
Valentin Sotov ◽  
David N. Douda ◽  
Daniela S. Ardelean ◽  
...  
Keyword(s):  
Mouse Model ◽  
Immune Cells ◽  
Vascular Endothelium ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Neutrophil Infiltration ◽  
Chronic Colitis ◽  
Resolution Of Inflammation ◽  
Pathological Angiogenesis ◽  
Persistent Inflammation

Endoglin is a coreceptor of the TGF-βsuperfamily predominantly expressed on the vascular endothelium and selective subsets of immune cells. We previously demonstrated thatEndoglinheterozygous (Eng+/−) mice subjected to dextran sulfate sodium (DSS) developed persistent gut inflammation and pathological angiogenesis. We now report that coliticEng+/−mice have low colonic levels of active TGF-β1, which was associated with reduced expression of thrombospondin-1, an angiostatic factor known to activate TGF-β1. We also demonstrate dysregulated expression of BMPER and follistatin, which are extracellular regulators of the TGF-βsuperfamily that modulate angiogenesis and inflammation. Heightened colonic levels of the neutrophil chemoattractant and proangiogenic factor, CXCL1, were also observed in DSS-treatedEng+/−mice. Interestingly, despite increased macrophage and neutrophil infiltration, a gut-specific reduction in expression of the key phagocytic respiratory burst enzymes, NADPH oxidase 2 (Nox-2) and myeloperoxidase, was seen inEng+/−mice undergoing persistent inflammation. Taken together, these findings suggest that endoglin is required for TGF-βsuperfamily mediated resolution of inflammation and fully functional myeloid cells.

scholarly journals Dextran sulfate sodium leads to chronic colitis and pathological angiogenesis in endoglin heterozygous mice

2010 ◽  
Vol 16 (11) ◽  
pp. 1859-1870 ◽  
Author(s):  
Mirjana Jerkic ◽  
Madonna Peter ◽  
Daniela Ardelean ◽  
Michael Fine ◽  
Moritz A. Konerding ◽  
...  
Keyword(s):  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Chronic Colitis ◽  
Pathological Angiogenesis

scholarly journals Characterization of the Synergistic Effect between Ligands of Opioid and Free Fatty Acid Receptors in the Mouse Model of Colitis

Molecules ◽  
2021 ◽  
Vol 26 (22) ◽  
pp. 6827
Author(s):  
Agata Binienda ◽  
Adam Makaro ◽  
Marcin Talar ◽  
Julia B. Krajewska ◽  
Aleksandra Tarasiuk ◽  
...  
Keyword(s):  
Mouse Model ◽  
Synergistic Effect ◽  
Immune Cells ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Intestinal Inflammation ◽  
Acute Colitis ◽  
Μ Opioid Receptor ◽  
Free Fatty Acid Receptors

Background: Recent studies suggest that lipids, including free fatty acids (FFAs), are necessary for proper μ opioid receptor (MOR) binding and that activation of opioid receptors (ORs) improves intestinal inflammation. The objective of the study was to investigate a possible interaction between the ORs and FFA receptors (FFARs) ligands in the colitis. Methods: The potential synergistic effect of ORs and FFARs ligands was evaluated using mouse model of acute colitis induced by dextran sulfate sodium (DSS, 4%). Compounds were injected intraperitoneally (i.p.) once or twice daily at the doses of 0.01 or 0.02 mg/kg body weight (BW) (DAMGO—an MOR agonist), 0.3 mg/kg BW (DPDPE—a δ OR (DOR) agonist) and 1 mg/kg BW (naloxone—a non-selective OR antagonist, GLPG 0974—a FFAR2 antagonist, GSK 137647—a FFAR4 agonist and AH 7614—a FFAR4 antagonist) for 4 days. Results: Myeloperoxidase (MPO) activity was significantly decreased after DAMGO (0.02 mg/kg BW) and GSK 137647 (1 mg/kg BW) administration and co-administration as compared to DSS group. Conclusions: Treatment with ligands of ORs and FFARs may affect the immune cells in the inflammation; however, no significant influence on the severity of colitis and no synergistic effect were observed.

Shikonin inhibits colitis-associated colorectal dysplasias in a mouse model of azoxymethane/dextran sulfate sodium colitis

Planta Medica ◽  
2012 ◽  
Vol 78 (11) ◽  
Author(s):  
JL Ríos ◽  
A Martí ◽  
I Andújar ◽  
RM Giner ◽  
MC Recio
Keyword(s):  
Mouse Model ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium

Prevention of Dextran Sulfate Sodium-induced Mouse Colitis by a Fungal Protein Ling Zhi-8 via Promoting the Barrier Function of Intestinal Epithelial Cells

2021 ◽  
Author(s):  
Yu-Huan Chen ◽  
Jenn-Yeu Shin ◽  
Hsiu-Mei Wei ◽  
Chi-Chen Lin ◽  
Linda Chia-Hui Yu ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Immune Cells ◽  
Ganoderma Lucidum ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Fungal Protein ◽  
Fungal Immunomodulatory Protein

A fungal immunomodulatory protein Ling Zhi-8 (LZ-8) isolated from Ganoderma lucidum (GL) regulates immune cells and inhibits tumor growth; however, the role of LZ-8 in intestinal epithelial cells (IECs) is...

scholarly journals Longitudinal Microbiome Analysis in a Dextran Sulfate Sodium-Induced Colitis Mouse Model

2021 ◽  
Vol 9 (2) ◽  
pp. 370
Author(s):  
Hyunjoon Park ◽  
Soyoung Yeo ◽  
Seokwon Kang ◽  
Chul Sung Huh
Keyword(s):  
Mouse Model ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Intestinal Bleeding ◽  
Cross Sectional ◽  
Microbiome Analysis ◽  
Inflammatory Bowel ◽  
Factor Design ◽  
The Individual

The role of the gut microbiota in the pathogenesis of inflammatory bowel disease (IBD) has been in focus for decades. Although metagenomic observations in patients/animal colitis models have been attempted, the microbiome results were still indefinite and broad taxonomic presumptions were made due to the cross-sectional studies. Herein, we conducted a longitudinal microbiome analysis in a dextran sulfate sodium (DSS)-induced colitis mouse model with a two-factor design based on serial DSS dose (0, 1, 2, and 3%) and duration for 12 days, and four mice from each group were sacrificed at two-day intervals. During the colitis development, a transition of the cecal microbial diversity from the normal state to dysbiosis and dynamic changes of the populations were observed. We identified genera that significantly induced or depleted depending on DSS exposure, and confirmed the correlations of the individual taxa to the colitis severity indicated by inflammatory biomarkers (intestinal bleeding and neutrophil-derived indicators). Of note, each taxonomic population showed its own susceptibility to the changing colitis status. Our findings suggest that an understanding of the individual susceptibility to colitis conditions may contribute to identifying the role of the gut microbes in the pathogenesis of IBD.

scholarly journals Dextran sulfate sodium mouse model of inflammatory bowel disease evaluated for systemic genotoxicity via blood micronucleus and Pig-a gene mutation assays

Mutagenesis ◽  
2020 ◽  
Vol 35 (2) ◽  
pp. 161-167
Author(s):  
Christopher Kirby ◽  
Ayesha Baig ◽  
Svetlana L Avlasevich ◽  
Dorothea K Torous ◽  
Shuchang Tian ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Mouse Model ◽  
Bowel Disease ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
High Dose ◽  
Significant Treatment ◽  
Blood Samples ◽  
Inflammatory Bowel ◽  
Blood Specimens

Abstract Inflammatory bowel disease (IBD) is an important risk factor for gastrointestinal cancers. Inflammation and other carcinogenesis-related effects at distal, tissue-specific sites require further study. In order to better understand if systemic genotoxicity is associated with IBD, we exposed mice to dextran sulfate sodium salt (DSS) and measured the incidence of micronucleated cells (MN) and Pig-a mutant phenotype cells in blood erythrocyte populations. In one study, 8-week-old male CD-1 mice were exposed to 0, 1, 2, 3 or 4% w/v DSS in drinking water. The 4-week in-life period was divided into four 1-week intervals—alternately on then off DSS treatment. Low volume blood samples were collected for MN analysis at the end of each week, and cardiac blood samples were collected at the end of the 4-week period for Pig-a analyses. The two highest doses of DSS were observed to induce significant increases in reticulocyte frequencies. Even so, no statistically significant treatment-related effects on the genotoxicity biomarkers were evident. While one high-dose mouse showed modestly elevated MN frequencies during the DSS treatment cycles, it also exhibited exceptionally high reticulocyte frequencies (e.g. 18.7% at the end of the second DSS cycle). In a second study, mice were treated with 0 or 4% DSS for 9–18 consecutive days. Exposure was continued until rectal bleeding or morbidity was evident, at which point the treatment was terminated and blood was collected for MN analysis. The Pig-a assay was conducted on samples collected 29 days after the start of treatment. The initial blood specimens showed highly elevated reticulocyte frequencies in DSS-exposed mice (mean ± SEM = 1.75 ± 0.10% vs. 13.04 ± 3.66% for 0 vs. 4% mice, respectively). Statistical analyses showed no treatment-related effect on MN or Pig-a mutant frequencies. Even so, the incidence of MN versus reticulocytes in the DSS-exposed mice were positively correlated (linear fit R2 = 0.657, P = 0.0044). Collectively, these results suggest that in the case of the DSS CD-1 mouse model, systemic effects include stress erythropoiesis but not remarkable genotoxicity. To the extent MN may have been slightly elevated in a minority of individual mice, these effects appear to be secondary, likely attributable to stimulated erythropoiesis.

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