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

ABSTRACT: 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-1? 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.

SUBMITTER: Nii T

PROVIDER: S-EPMC7844332 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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

Nii Takahiro T Bungo Takashi T Isobe Naoki N Yoshimura Yukinori Y

Frontiers in physiology 20210115

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 envir ...[more]

PMID: 33519513

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Project description:BackgroundG protein-coupled receptor 35 (GPR35) is an orphan receptor and is vastly expressed in immune cells and gastrointestinal cells, suggesting the potential physiological importance of GPR35 in these cells. Here, we tested the hypothesis that the lack of GPR35 expression in the colon mucosa exacerbates the severity of dextran sulfate sodium (DSS)-induced experimental colitis in mice.MethodsColitis was induced in GPR35 wild-type (GPR35+/+) and GPR35 knockout (GPR35-/-) mice through the administration of DSS in drinking water for 5 days followed by regular facility water for 1 day. Induction of colitis was evaluated by measuring relative body weight loss, clinical illness scores, and morphological changes in the colon. Abolition of Gpr35 gene expression in the colon mucosa of GPR35-/- mice was confirmed by quantitative real-time PCR (qPCR). Gene expressions of inflammatory and tissue remodeling cytokines were detected by qPCR. Human colorectal epithelial Caco cells were transfected with siRNA against GPR35 before treated with 1% DSS in vitro. Protein expressions were measured using Western blot.ResultsGPR35-/- mice receiving DSS showed a significantly worsened colitis disease with profound loss of body weight and a considerable amount of severe clinical illness compared to GPR35+/+ mice that received DSS. The histology of colon sections from GPR35-/- mice showed extensive pathological changes including submucosal edema, diffuse ulcerations, and evidence of complete loss of crypts compared to wild-type mice. The mean histopathological score was significantly higher in GPR35-/- mice as compared to GPR35+/+ mice. The qPCR data revealed significant expression of pro-inflammatory and tissue remodeling cytokines in GPR35-/- colon mucosa, including IL-1β, CXCL1, CXCL2, CCL2, HMGB1, TGFβ1, TGFβ3, MMP1/9/12. The protein expressions of Zonula occludens-1, E-cadherin, Claudin1 were decreased upon knocking down GPR35 with or without 1% DSS treatment.ConclusionsOur experimental data suggest that lack of GPR35 resulted in worsened disease outcome in DSS-induced experimental colitis, indicating that GPR35 could play a crucial role in protecting from colonic inflammation and serve as a therapeutic target.

Project description:BACKGROUND:Ulcerative colitis causes recurring intestinal mucosal injury and sustained inflammation, increasing the likelihood of colorectal cancer (CRC) development. Dietary red raspberry (RB) is a rich source of phytonutrients known to have anti-inflammatory activity; however, the role of RB on CRC prevention in chronic colitis has not been examined. OBJECTIVE:This study examined the effects of dietary RB supplementation on inflammation, epithelium repair, and oncogenic signaling in dextran sulfate sodium (DSS)-induced chronic colitis in mice. METHODS:Six-week-old male C57BL/6J mice were fed a control or RB (5% of dry feed weight; n = 12/group) diet for 10 wk. Starting from the fourth week, mice were administered 2 repeated cycles of 1% DSS (7-d DSS treatment plus 14-d recovery) and were monitored daily for disease activity index (DAI) score. Colonic tissues were collected at the end of the study for histochemical, immunohistochemical, and biochemical analysis of inflammation, differentiation and proliferation markers. RESULTS:RB supplementation reduced the DAI score and histologic damage (by 38.9%; P ? 0.01), expression of inflammatory mediators (by 20-70%; P ? 0.01), infiltration of CD4 T cells (by 50%; P ? 0.05), and ?4?7 integrin and related adhesion molecules (by 33.3%; P ? 0.01). Furthermore, RB supplementation facilitated epithelium repair, as evidenced by enhanced goblet cell density, expression of transcription factors including Kruppel-like factor 4 (Klf4) and Hairy and enhancer of split 1 (Hes1), terminal differentiation markers, mucin 2 (Muc2), and intestinal alkaline phosphatase (by 20-200%; P ? 0.01). Conversely, proliferating cell nuclear antigen (by 70%; P ? 0.01), ?-catenin, and signal transducer and activator of transcription 3 (STAT3) signaling (by 19-33%; P ? 0.05) were reduced by RB supplementation. In addition, RB supplementation enhanced p53 stability (by 53%) and reduced oncogenic gene expression (by 50-60%). CONCLUSION:RB supplementation reduced DAI score and the risk of CRC development during recurring colitis in mice, suggesting that RB is a possible dietary supplement for patients with ulcerative colitis and related gut inflammatory diseases.

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Dataset Information

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

Publications

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

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