Effect of Oral Administration of 3,3′-Diindolylmethane on Dextran Sodium Sulfate-Induced Acute Colitis in Mice

2016 ◽  
Vol 64 (41) ◽  
pp. 7702-7709 ◽  
Author(s):  
Eun-Joo Jeon ◽  
Munkhtugs Davaatseren ◽  
Jin-Taek Hwang ◽  
Jae Ho Park ◽  
Haeng Jeon Hur ◽  
...  
Keyword(s):  
Oral Administration ◽  
Sodium Sulfate ◽  
Dextran Sodium Sulfate ◽  
Acute Colitis

scholarly journals Slight Disruption in Intestinal Environment by Dextran Sodium Sulfate Reduces Egg Yolk Size Through Disfunction of Ovarian Follicle Growth

2021 ◽  
Vol 11 ◽  
Author(s):  
Takahiro Nii ◽  
Takashi Bungo ◽  
Naoki Isobe ◽  
Yukinori Yoshimura
Keyword(s):  
Gene Expression ◽  
Oral Administration ◽  
Blood Plasma ◽  
Sodium Sulfate ◽  
Egg Production ◽  
Laying Hens ◽  
Ovarian Follicle ◽  
Egg Yolk ◽  
Dextran Sodium Sulfate ◽  
Intestinal Environment

Intestinal environments such as microbiota, mucosal barrier function, and cytokine production affect egg production in laying hens. Dextran sodium sulfate (DSS) is an agent that disrupts the intestinal environment. Previously, we reported that the oral administration of dextran sodium sulfate (DSS: 0.9 g/kg BW) for 5 days caused severe intestinal inflammation in laying hens. However, the DSS concentration in the previous study was much higher to induce a milder disruption of the intestinal environment without heavy symptoms. Thus, the goal of this study was to determine the effects of a lower dose of DSS on the intestinal environment and egg production in laying hens. White Leghorn laying hens (330-day old) were oral administered with or without 0.225 g DSS/kg BW for 28 days (DSS and control group: n = 7 and 8, respectively). Weekly we collected all laid eggs and blood plasma samples. Intestinal tissues, liver, ovarian follicles, and the anterior pituitary gland were collected 1 day after the final treatment. Lower concentrations of orally administered DSS caused (1) a decrease in the ratio of villus height/crypt depth, occludin gene expressions in large intestine and cecal microbiota diversity, (2) a decrease in egg yolk weight, (3) an increase in VLDLy in blood plasma, (4), and enhanced the egg yolk precursor accumulation in the gene expression pattern in the follicular granulosa layer, (5) an increase in FSH and IL-1β gene expression in the pituitary gland, and (6) an increase in concentration of plasma lipopolysaccharide binding protein. These results suggested that the administration of the lower concentration of DSS caused a slight disruption in the intestinal environment. This disruption included poor intestinal morphology and decreased cecal microbiome diversity. The change in the intestinal environment decreases egg yolk size without decreasing the VLDLy supply from the liver. The decrease in egg yolk size is likely to be caused by the dysfunction of egg-yolk precursor uptake in ovarian follicles. In conclusion, the oral administration of a lower dose of DSS is an useful method to cause slight disruptions of intestinal environment, and the intestinal condition decreases egg yolk size through disfunction of ovarian follicle.

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.

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