scholarly journals Production of lipid mediators across different disease stages of dextran sodium sulfate-induced colitis in mice

2018 ◽  
Vol 59 (4) ◽  
pp. 586-595 ◽  
Author(s):  
Taiki Hamabata ◽  
Tatsuro Nakamura ◽  
Sakura Masuko ◽  
Shingo Maeda ◽  
Takahisa Murata
Keyword(s):  
Fatty Acid ◽  
Sodium Sulfate ◽  
Acute Inflammation ◽  
Intestinal Inflammation ◽  
Recovery Phase ◽  
Lipid Mediators ◽  
Dextran Sodium Sulfate ◽  
Prostaglandin E ◽  
Induction Phase ◽  
Colon Tissue

Although several studies have revealed the role of different lipid mediators in colitis, the comprehensive analysis of their production across different phases of colitis remained unclear. Here, we performed the following analysis in the dextran sodium sulfate (DSS)-induced colitis model using LC-MS/MS. Oral administration of 2% DSS in mice for 4 days resulted in severe intestinal inflammation by day 7, which gradually subsided by day 18. Based on the disease scoring index (assigned on the basis of fecal condition and weight loss), we defined the phases of colitis as induction (days 0–4), acute inflammation (days 4–7), recovery (days 7–9), and late recovery (days 9–18). Across all phases, 58 lipid mediators were detected in the inflamed colon tissue. In the induction phase, the production of n-6 fatty acid-derived prostaglandin E2 and thromboxane B2 increased by ∼2-fold. In the acute inflammation phase, the production of n-6 fatty acid-derived leukotrienes increased by >10-fold, while that of n-3 fatty acid-derived hydroxyeicosapentaenoic acids and dihydroxyeicosatetraenoic acids decreased. In the recovery phase, a precursor of protectin D1 (17-hydroxydocosahexaenoic acid) increased over 3-fold. These observations suggested dynamic changes in the production of lipid mediators across different phases of the disease and their potential regulation in healing colitis.

scholarly journals Ethanol Extract ofCordyceps militarisGrown on Germinated Soybeans Attenuates Dextran-Sodium-Sulfate- (DSS-) Induced Colitis by Suppressing the Expression of Matrix Metalloproteinases and Inflammatory Mediators

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Dong Ki Park ◽  
Hye-Jin Park
Keyword(s):  
Matrix Metalloproteinases ◽  
Inflammatory Mediators ◽  
Sodium Sulfate ◽  
Activity Index ◽  
Disease Activity Index ◽  
Ethanol Extract ◽  
Treated Group ◽  
Dextran Sodium Sulfate ◽  
Protective Agent ◽  
Colon Tissue

The effect ofCordyceps militaris(CM) grown on germinated soybeans (GSC) in the inflammatory bowel disease (IBD) model was studied. To demonstrate the preventive effect of GSC extract in a dextran-sodium-sulfate- (DSS-) induced acute colitis mouse model, GSC was administered 2 days before DSS coadministration. GSC significantly suppressed DSS-induced disease activity index (DAI) as well as histopathological scores, compared to control or CM-treated group. To elucidate the anti-IBD activity of GSC, we checked the level of matrix metalloproteinases (MMPs) and inflammatory mediators. GSC extract decreased the level of MMP-3 and -9 mRNAs and p53 proteins. The level and activity of LPS-induced MMP-9 were reduced in GSC-treated RAW264.7 cells. It also attenuated the level of inducible nitric oxide synthase (iNOS) and tumor necrosis factor- (TNF-)αmRNAs both in colon tissue and in macrophage cells. These results suggest that GSC can be applied as a protective agent against IBDs.

Malt1 blocks IL-1β production by macrophages in vitro and limits dextran sodium sulfate-induced intestinal inflammation in vivo

2018 ◽  
Vol 104 (3) ◽  
pp. 557-572 ◽  
Author(s):  
Mahdis Monajemi ◽  
Yvonne C. F. Pang ◽  
Saelin Bjornson ◽  
Susan C. Menzies ◽  
Nico van Rooijen ◽  
...  
Keyword(s):  
Sodium Sulfate ◽  
Intestinal Inflammation ◽  
Dextran Sodium Sulfate

scholarly journals Acetylsalicylic Acid Reduces the Severity of Dextran Sodium Sulfate-Induced Colitis and Increases the Formation of Anti-Inflammatory Lipid Mediators

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Thomas Köhnke ◽  
Beate Gomolka ◽  
Süleyman Bilal ◽  
Xiangzhi Zhou ◽  
Yanping Sun ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Acetylsalicylic Acid ◽  
Bowel Disease ◽  
Sodium Sulfate ◽  
Lipid Mediators ◽  
Dextran Sodium Sulfate ◽  
Cyclooxygenase Inhibitors ◽  
Omega 3 ◽  
Inflammatory Bowel ◽  
Anti Inflammatory

The role of non-steroidal anti-inflammatory drugs in inflammatory bowel disease is controversial, as they have been implicated in disease aggravation. Different from other cyclooxygenase inhibitors, acetylsalicylic acid (ASA) enhances the formation of anti-inflammatory and proresolution lipoxins derived from arachidonic acid as well as resolvins from omega-3 polyunsaturated fatty acids such as docosahexaenoic acid (DHA). In this study, we examined the effect of ASA on murine dextran sodium sulfate colitis. A mouse magnetic resonance imaging (MRI) protocol and post mortem assessment were used to assess disease severity, and lipid metabolites were measured using liquid chromatography-coupled tandem mass spectrometry. Decreased colitis activity was demonstrated by phenotype and MRI assessment in mice treated with ASA, and confirmed in postmortem analysis. Analysis of lipid mediators showed sustained formation of lipoxin A4 and an increase of DHA-derived 17-hydroxydocosahexaenoic acid (17-HDHA) after treatment with ASA. Furthermore,in vitroexperiments in RAW264.7 murine macrophages demonstrated significantly increased phagocytosis activity after incubation with 17-HDHA, supporting its proresolution effect. These results show a protective effect of ASA in a murine colitis model and could give a rationale for a careful reassessment of ASA therapy in patients with inflammatory bowel disease and particularly ulcerative colitis, possibly combined with DHA supplementation.

MyD88-deficient mice develop severe intestinal inflammation in dextran sodium sulfate colitis

2005 ◽  
Vol 40 (1) ◽  
pp. 16-23 ◽  
Author(s):  
Akihiro Araki ◽  
Takanori Kanai ◽  
Takahiro Ishikura ◽  
Shin Makita ◽  
Koji Uraushihara ◽  
...  
Keyword(s):  
Sodium Sulfate ◽  
Intestinal Inflammation ◽  
Dextran Sodium Sulfate ◽  
Deficient Mice

scholarly journals Interleukin-10 is Differentially Expressed in the Small Intestine and the Colon Experiencing Chronic Inflammation and Ulcerative Colitis Induced by Dextran Sodium Sulfate in Young Pigs

2017 ◽  
pp. 147-162 ◽  
Author(s):  
D. LACKEYRAM ◽  
D. YOUNG ◽  
C. J. KIM ◽  
C. YANG ◽  
T. L. ARCHBOLD ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Chronic Inflammation ◽  
Chronic Ulcerative Colitis ◽  
Sodium Sulfate ◽  
Intestinal Inflammation ◽  
Interleukin 10 ◽  
Dextran Sodium Sulfate ◽  
Mrna Abundance ◽  
Control Group ◽  
Young Pigs

Intestinal inflammation induced with dextran sodium sulfate (DSS) is used to study acute or chronic ulcerative colitis in animal models. Decreased gut tissue anti-inflammatory cytokine IL-10 concentration and mRNA abundance are associated with the development of chronic bowel inflammation. Twelve piglets of 3 days old were fitted with an intragastric catheter and randomly allocated into control and DSS groups by administrating either sterile saline or 1.25 g of DSS/kg body weight (BW) in saline per day, respectively, for 10 days. Growth rate and food conversion efficiency were reduced (p<0.05) in the DSS piglets compared with the control group. Quantitative histopathological grading of inflammation in the jejunum and colon collectively showed that the DSS treatment resulted in 12 fold greater (p<0.05) inflammation severity scoring in the colon than in the jejunum, indicative of chronic ulcerative colitis in the colon. Upper gut permeability endpoint was 27.4 fold higher (p<0.05) in the DSS group compared with the control group. The DSS group had higher concentrations and mRNA abundances (p<0.05) of TNF- and IL-6 in the jejunal and colonic tissues compared with the control group. Colonic concentration and mRNA abundance of IL-10 were reduced (p<0.05), however, jejunal IL-10 mRNA abundance was increased (p<0.05) in the DSS group compared with the control group. In conclusion, administration of DSS at 1.25 g/kg BW for 10 days respectively induced acute inflammation in the jejunum and chronic inflammation and ulcerative colitis in the colon with substantially decreased colonic concentration and mRNA abundance of IL-10 in the young pigs, mimicking the IL-10 expression pattern in humans associated with chronic bowel inflammation.

scholarly journals Lactobacillus bulgaricus inhibits colitis-associated cancer via a negative regulation of intestinal inflammation in azoxymethane/dextran sodium sulfate model

2020 ◽  
Vol 26 (43) ◽  
pp. 6782-6794
Author(s):  
Denise Sayuri Calheiros Silveira ◽  
Luciana Chain Veronez ◽  
Luís Carlos Lopes-Júnior ◽  
Elen Anatriello ◽  
Mariângela Ottoboni Brunaldi ◽  
...  
Keyword(s):  
Sodium Sulfate ◽  
Intestinal Inflammation ◽  
Negative Regulation ◽  
Dextran Sodium Sulfate ◽  
Lactobacillus Bulgaricus

Chickpea supplementation prior to colitis onset reduces inflammation in dextran sodium sulfate-treated C57Bl/6 male mice

2018 ◽  
Vol 43 (9) ◽  
pp. 893-901 ◽  
Author(s):  
Jennifer M. Monk ◽  
Wenqing Wu ◽  
Laurel H. McGillis ◽  
Hannah R. Wellings ◽  
Amber L. Hutchinson ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Sodium Sulfate ◽  
Clinical Symptoms ◽  
Basal Diet ◽  
Serum Levels ◽  
Dextran Sodium Sulfate ◽  
Male Mice ◽  
Acute Colitis ◽  
Colon Tissue ◽  
Necrosis Factor Alpha

The potential for a chickpea-supplemented diet (rich in fermentable nondigestible carbohydrates and phenolic compounds) to modify the colonic microenvironment and attenuate the severity of acute colonic inflammation was investigated. C57Bl/6 male mice were fed a control basal diet or basal diet supplemented with 20% cooked chickpea flour for 3 weeks prior to acute colitis onset induced by 7-day exposure to dextran sodium sulfate (DSS; 2% w/v in drinking water) and colon and serum levels of inflammatory mediators were assessed. Despite an equal degree of DSS-induced epithelial barrier histological damage and clinical symptoms between dietary groups, biomarkers of the ensuing inflammatory response were attenuated by chickpea pre-feeding, including reduced colon tissue activation of nuclear factor kappa B and inflammatory cytokine production (tumor necrosis factor alpha and interleukin (IL)-18). Additionally, colon protein expression of anti-inflammatory (IL-10) and epithelial repair (IL-22 and IL-27) cytokines were increased by chickpea pre-feeding. Furthermore, during acute colitis, chickpea pre-feeding increased markers of enhanced colonic function, including Relmβ and IgA gene expression. Collectively, chickpea pre-feeding modulated the baseline function of the colonic microenvironment, whereby upon induction of acute colitis, the severity of the inflammatory response was attenuated.

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