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      Intestinal inflammation induced by dextran sodium sulphate causes liver inflammation and lipid metabolism disfunction in laying hens

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          Abstract

          Gut inflammation caused by various factors including microbial infection leads to disorder of absorption of dietary nutrients and decrease in egg production in laying hens. We hypothesized that intestinal inflammation may affect egg production in laying hens through its impact on liver function. Dextran sodium sulphate ( DSS) is known to induce intestinal inflammation in mammals, but whether it also induces inflammation in laying hens is not known. The goal of this study was to assess whether oral administration of DSS is a useful model of intestinal inflammation in laying hens and to characterize the effects of intestinal inflammation on egg production using this model. White Leghorn hens (350-day old) were administrated with or without 0.9 g of DSS/kg BW in drinking water for 5 D (n = 8, each). All laid eggs were collected, and their whole and eggshell weights were recorded. Blood was collected every day and used for biochemical analysis. Liver and intestinal tissues (duodenum, jejunum, ileum, cecum, cecal-tonsil, and colon) were collected 1 D after the final treatment. These tissue samples were used for histological analysis and PCR analysis. Oral administration of DSS in laying hens caused 1) histological disintegration of the cecal mucosal epithelium and increased monocyte/macrophage infiltration and IL-1β, IL-6, CXCLi2, IL-10, and TGFβ-4 gene expression; 2) decreased egg production; 3) increased leukocyte infiltration and IL-1β, CXCLi2, and IL-10 expression in association with a high frequency of lipopolysaccharide-positive cells in the liver; and 4) decreased expression of genes related to lipid synthesis, lipoprotein uptake, and yolk precursor production. These results suggested that oral administration of DSS is a useful method for inducing intestinal inflammation in laying hens, and intestinal inflammation may reduce egg production by disrupting egg yolk precursor production in association with liver inflammation.

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          Chemically induced mouse models of intestinal inflammation.

          Animal models of intestinal inflammation are indispensable for our understanding of the pathogenesis of Crohn disease and ulcerative colitis, the two major forms of inflammatory bowel disease in humans. Here, we provide protocols for establishing murine 2,4,6-trinitro benzene sulfonic acid (TNBS)-, oxazolone- and both acute and chronic dextran sodium sulfate (DSS) colitis, the most widely used chemically induced models of intestinal inflammation. In the former two models, colitis is induced by intrarectal administration of the covalently reactive reagents TNBS/oxazolone, which are believed to induce a T-cell-mediated response against hapten-modified autologous proteins/luminal antigens. In the DSS model, mice are subjected several days to drinking water supplemented with DSS, which seems to be directly toxic to colonic epithelial cells of the basal crypts. The procedures for the hapten models of colitis and acute DSS colitis can be accomplished in about 2 weeks but the protocol for chronic DSS colitis takes about 2 months.
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            A novel method in the induction of reliable experimental acute and chronic ulcerative colitis in mice.

            Acute and chronic experimental ulcerative colitis models were produced in mice by providing them with drinking water containing synthetic dextran sulfate sodium. Mice that developed acute colitis showed signs of diarrhea, gross rectal bleeding, and weight loss within 6-10 days after ingesting 3%-10% dextran sulfate sodium. On postmortem examination, multiple erosions and inflammatory changes including crypt abscesses were found on the left side of the large intestine. Mice that developed chronic colitis showed signs of erosions, prominent regenerations of the colonic mucosa including dysplasia, shortening of the large intestine, and frequent formation of lymphoid follicles after 5 administration cycles, where each cycle was composed of 7 days' consumption of drinking water containing 5% dextran sulfate sodium followed by 10 days' consumption of distilled water. The population of intestinal microflora, Bacteroides distasonis and Clostridium spp., increased significantly in mice with acute and chronic ulcerative colitis. Further, morphological studies suggest that the administered dextran sulfate sodium was partially phagocytized by macrophages in the colonic mucosa.
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              Dextran Sodium Sulphate Colitis Mouse Model: Traps and Tricks

              Inflammatory bowel disease (IBD) is a complex multifactorial disease of unknown etiology. Thus, dozens of different animal models of IBD have been developed in past decades. Animal models of IBD are valuable and indispensable tools that provide a wide range of options for investigating involvement of various factors into the pathogenesis of IBD and to evaluate different therapeutic options. However, the dextran sulphate sodium (DSS-) induced colitis model has some advantages when compared to other animal models of colitis. It is well appreciated and widely used model of inflammatory bowel disease because of its simplicity. It has many similarities to human IBD, which are mentioned in the paper. In spite of its simplicity and wide applicability, there are also traps that need to be taken into account when using DSS model. As demonstrated in the present paper, various factors may affect susceptibility to DSS-induced lesions and modify results.
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                Author and article information

                Contributors
                Journal
                Poult Sci
                Poult Sci
                Poultry Science
                Elsevier
                0032-5791
                1525-3171
                22 January 2020
                March 2020
                22 January 2020
                : 99
                : 3
                : 1663-1677
                Affiliations
                []Graduate School of Integrated Science for Life, Hiroshima University, Higashi-Hiroshima, Japan
                []Research Center for Animal Science, Hiroshima University, Higashi-Hiroshima, Japan
                Author notes
                [1 ]Corresponding author: tanii@ 123456hiroshima-u.ac.jp
                Article
                S0032-5791(19)57825-7
                10.1016/j.psj.2019.11.028
                7587789
                32111331
                e5e85e78-f863-4eda-ba0b-bd19a6658442
                © 2019 Published by Elsevier Inc. on behalf of Poultry Science Association Inc.

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 19 August 2019
                : 7 November 2019
                Categories
                Physiology and Reproduction

                intestinal inflammation,egg production,liver inflammation,dextran sodium sulphate,egg yolk precursor

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