Oral priming with oligodeoxynucleotide particles from Lactobacillus rhamnosus GG attenuates symptoms of dextran sodium sulfate‐induced acute colitis in mice

2020 ◽  
Vol 91 (1) ◽  
Author(s):  
Suguru Shigemori ◽  
Fu Namai ◽  
Tasuku Ogita ◽  
Takashi Sato ◽  
Takeshi Shimosato
Keyword(s):  
Sodium Sulfate ◽  
Lactobacillus Rhamnosus ◽  
Dextran Sodium Sulfate ◽  
Acute Colitis ◽  
Lactobacillus Rhamnosus Gg

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.

scholarly journals Milk Fat Globule-EGF Factor 8 Is a Critical Protein for Healing of Dextran Sodium Sulfate-Induced Acute Colitis in Mice

2011 ◽  
Vol 17 (5-6) ◽  
pp. 502-507 ◽  
Author(s):  
Ashish Chogle ◽  
Heng-Fu Bu ◽  
Xiao Wang ◽  
Jeffrey B Brown ◽  
Pauline M Chou ◽  
...  
Keyword(s):  
Sodium Sulfate ◽  
Milk Fat ◽  
Dextran Sodium Sulfate ◽  
Acute Colitis ◽  
Milk Fat Globule ◽  
Fat Globule

scholarly journals G protein-coupled receptor kinase-2-deficient mice are protected from dextran sodium sulfate-induced acute colitis

2018 ◽  
Vol 50 (6) ◽  
pp. 407-415 ◽  
Author(s):  
Michael D. Steury ◽  
Ho Jun Kang ◽  
Taehyung Lee ◽  
Peter C. Lucas ◽  
Laura R. McCabe ◽  
...  
Keyword(s):  
G Protein ◽  
Knockout Mice ◽  
Sodium Sulfate ◽  
Immune Cell ◽  
Dextran Sodium Sulfate ◽  
Receptor Kinase ◽  
G Protein Coupled Receptor ◽  
Acute Colitis ◽  
Inflammatory Genes ◽  
G Protein Coupled

G protein-coupled receptor kinase 2 (GRK2) is a serine/threonine kinase and plays a key role in different disease processes. Previously, we showed that GRK2 knockdown enhances wound healing in colonic epithelial cells. Therefore, we hypothesized that ablation of GRK2 would protect mice from dextran sodium sulfate (DSS)-induced acute colitis. To test this, we administered DSS to wild-type (GRK2+/+) and GRK2 heterozygous (GRK+/−) mice in their drinking water for 7 days. As predicted, GRK2+/− mice were protected from colitis as demonstrated by decreased weight loss (20% loss in GRK2+/+ vs. 11% loss in GRK2+/−). lower disease activity index (GRK2+/+ 9.1 vs GRK2+/− 4.1), and increased colon lengths (GRK2+/+ 4.7 cm vs GRK2+/− 5.3 cm). To examine the mechanisms by which GRK2+/− mice are protected from colitis, we investigated expression of inflammatory genes in the colon as well as immune cell profiles in colonic lamina propria, mesenteric lymph node, and in bone marrow. Our results did not reveal differences in immune cell profiles between the two genotypes. However, expression of inflammatory genes was significantly decreased in DSS-treated GRK2+/− mice compared with GRK2+/+. To understand the mechanisms, we generated myeloid-specific GRK2 knockout mice and subjected them to DSS-induced colitis. Similar to whole body GRK2 heterozygous knockout mice, myeloid-specific knockout of GRK2 was sufficient for the protection from DSS-induced colitis. Together our results indicate that deficiency of GRK2 protects mice from DSS-induced colitis and further suggests that the mechanism of this effect is likely via GRK2 regulation of inflammatory genes in the myeloid cells.

scholarly journals Th17 Responses Are Not Induced in Dextran Sodium Sulfate Model of Acute Colitis

2011 ◽  
Vol 11 (6) ◽  
pp. 416 ◽  
Author(s):  
Yoon Suk Kim ◽  
Min Ho Lee ◽  
Ahn Seung Ju ◽  
Ki-Jong Rhee
Keyword(s):  
Sodium Sulfate ◽  
Dextran Sodium Sulfate ◽  
Acute Colitis
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