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takeshi azuma & masaru yoshida month download article/chapter attenuated dss-induced colitis tgf-beta-related signaling exhibits anti-inflammatory properties arnt-sim homology superfamily cell type-specific expression benzene-induced hematopoietic toxicity basic helix-loop-helix/ dextran sodium sulfate ligand-activated transcription factor article digestive diseases arylhydrocarbon receptor-dependent induction lipopolysaccharide-induced septic shock beta-naphthoflavone-induced rats dioxin toxicity–xenobiotic misappropriation inflammatory responses evoked th1/th2 balance aryl hydrocarbon receptor aryl hydrocarbon receptor dioxin-binding ah receptor full article pdf yoshiaki fujii-kuriyama aromatic hydrocarbon receptor related subjects privacy choices/manage cookies dss-induced colitis tnbs-induced colitis mouse colitis mediated perpetuate experimental colitis chronic ulcerative colitis suppresses th2 differentiation intestinal epithelial barrier reliable experimental acute de man jg genetically engineered c57bl/6 genetic model systems bone marrow cells nf-kappab interactions experimental autoimmune uveoretinitis colonic epithelial repair inflammatory dendritic cells langerhans cell maturation inflammatory bowl disease inflammatory bowel disease β-naphthoflavone organ disorders including colon epithelium liver preneoplastic lesions aryl hydrocarbon

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         headline:A Role of the Aryl Hydrocarbon Receptor in Attenuation of Colitis
         description:The aryl hydrocarbon receptor (AhR), which is a member of the basic helix-loop-helix/Per-Arnt-Sim homology superfamily, plays an important role in multiple biological functions, and AhR knockout (AhR KO) animals suffer from a variety of organ disorders including a decline in the efficacy of their immune system. In addition, AhR activation is known to aid the maintenance of homeostasis in vivo. In this study, we investigated whether AhR is functionally associated with intestinal immunity. In in vivo experiments, it was found that dextran sodium sulfate (DSS)-evoked colitis was more severe in AhR KO mice than in C57BL/6J wild type mice. It was also revealed that the administration of DSS increased the expression levels of AhR and CYP1A1 mRNA in the colon epithelium. In addition, oral administration of β-naphthoflavone (βNF), a non-toxic agonist of AhR, suppressed the pathogenesis of DSS-induced colitis. βNF also attenuated DSS-induced colitis. In cell culture experiments, downregulation of AhR in human colon carcinoma SW480 cells enhanced the inflammatory responses evoked by lipopolysaccharide (LPS), and furthermore, AhR activation attenuated LPS-induced inflammatory responses, suggesting that AhR expressing intestinal epithelial cells are involved in the prevention of colitis. Our findings about the potential role of AhR activators in epithelial immune regulation aid our understanding of mucosal homeostasis and inflammatory bowl disease (IBD) and suggest that AhR activation has therapeutic value for the treatment of IBD.
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      headline:A Role of the Aryl Hydrocarbon Receptor in Attenuation of Colitis
      description:The aryl hydrocarbon receptor (AhR), which is a member of the basic helix-loop-helix/Per-Arnt-Sim homology superfamily, plays an important role in multiple biological functions, and AhR knockout (AhR KO) animals suffer from a variety of organ disorders including a decline in the efficacy of their immune system. In addition, AhR activation is known to aid the maintenance of homeostasis in vivo. In this study, we investigated whether AhR is functionally associated with intestinal immunity. In in vivo experiments, it was found that dextran sodium sulfate (DSS)-evoked colitis was more severe in AhR KO mice than in C57BL/6J wild type mice. It was also revealed that the administration of DSS increased the expression levels of AhR and CYP1A1 mRNA in the colon epithelium. In addition, oral administration of β-naphthoflavone (βNF), a non-toxic agonist of AhR, suppressed the pathogenesis of DSS-induced colitis. βNF also attenuated DSS-induced colitis. In cell culture experiments, downregulation of AhR in human colon carcinoma SW480 cells enhanced the inflammatory responses evoked by lipopolysaccharide (LPS), and furthermore, AhR activation attenuated LPS-induced inflammatory responses, suggesting that AhR expressing intestinal epithelial cells are involved in the prevention of colitis. Our findings about the potential role of AhR activators in epithelial immune regulation aid our understanding of mucosal homeostasis and inflammatory bowl disease (IBD) and suggest that AhR activation has therapeutic value for the treatment of IBD.
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            address:
               name:Division of Metabolomics Research, Kobe University Graduate School of Medicine, Kobe, Japan
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Division of Gastroenterology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Hyogo, Japan
      name:Division of Gastroenterology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Hyogo, Japan
      name:The Integrated Center for Mass Spectrometry, Kobe University Graduate School of Medicine, Kobe, Japan
      name:Division of Gastroenterology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Hyogo, Japan
      name:Division of Gastroenterology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Hyogo, Japan
      name:Division of Gastroenterology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Hyogo, Japan
      name:Division of Gastroenterology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Hyogo, Japan
      name:Division of Gastroenterology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Hyogo, Japan
      name:Department of Agrobioscience, Kobe University Graduate School of Agricultural Science, Kobe, Japan
      name:Institute of Molecular and Cellular Biosciences, The University of Tokyo, Bunkyo-ku, Japan
      name:Division of Gastroenterology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Hyogo, Japan
      name:Division of Gastroenterology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Hyogo, Japan
      name:The Integrated Center for Mass Spectrometry, Kobe University Graduate School of Medicine, Kobe, Japan
      name:Division of Metabolomics Research, Kobe University Graduate School of Medicine, Kobe, Japan
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