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  • 1
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    Prokaryotic regulation of epithelial responses by inhibition of IkappaB-alpha ubiquitination (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-09-01
    Description: Epithelia of the vertebrate intestinal tract characteristically maintain an inflammatory hyporesponsiveness toward the lumenal prokaryotic microflora. We report the identification of enteric organisms (nonvirulent Salmonella strains) whose direct interaction with model human epithelia attenuate synthesis of inflammatory effector molecules elicited by diverse proinflammatory stimuli. This immunosuppressive effect involves inhibition of the inhibitor kappaB/nuclear factor kappaB (IkappaB/NF-kappaB) pathway by blockade of IkappaB-alpha degradation, which prevents subsequent nuclear translocation of active NF-kappaB dimer. Although phosphorylation of IkappaB-alpha occurs, subsequent polyubiquitination necessary for regulated IkappaB-alpha degradation is completely abrogated. These data suggest that prokaryotic determinants could be responsible for the unique tolerance of the gastrointestinal mucosa to proinflammatory stimuli.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Neish, A S -- Gewirtz, A T -- Zeng, H -- Young, A N -- Hobert, M E -- Karmali, V -- Rao, A S -- Madara, J L -- DK-35932/DK/NIDDK NIH HHS/ -- DK-47662/DK/NIDDK NIH HHS/ -- DK09800/DK/NIDDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 2000 Sep 1;289(5484):1560-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Epithelial Pathobiology Unit, Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA. aneish@emory.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10968793" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Nucleus/metabolism ; Cysteine Proteinase Inhibitors/pharmacology ; Cytoskeletal Proteins/metabolism ; DNA-Binding Proteins/*metabolism ; Dimerization ; Humans ; *I-kappa B Proteins ; Inflammation Mediators/pharmacology ; Interleukin-8/genetics/metabolism ; Intestinal Mucosa/*metabolism/*microbiology ; Leupeptins/pharmacology ; Ligases/metabolism ; NF-kappa B/genetics/*metabolism ; Phosphorylation ; Salmonella/pathogenicity/*physiology ; Salmonella typhimurium/pathogenicity/physiology ; *Trans-Activators ; Transcription Factor RelA ; Tumor Cells, Cultured ; Tumor Necrosis Factor-alpha/pharmacology ; Ubiquitin-Protein Ligases ; Ubiquitins/metabolism ; beta Catenin
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Metabolic syndrome and altered gut microbiota in mice lacking Toll-like receptor 5 (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-03-06
    Description: Metabolic syndrome is a group of obesity-related metabolic abnormalities that increase an individual's risk of developing type 2 diabetes and cardiovascular disease. Here, we show that mice genetically deficient in Toll-like receptor 5 (TLR5), a component of the innate immune system that is expressed in the gut mucosa and that helps defend against infection, exhibit hyperphagia and develop hallmark features of metabolic syndrome, including hyperlipidemia, hypertension, insulin resistance, and increased adiposity. These metabolic changes correlated with changes in the composition of the gut microbiota, and transfer of the gut microbiota from TLR5-deficient mice to wild-type germ-free mice conferred many features of metabolic syndrome to the recipients. Food restriction prevented obesity, but not insulin resistance, in the TLR5-deficient mice. These results support the emerging view that the gut microbiota contributes to metabolic disease and suggest that malfunction of the innate immune system may promote the development of metabolic syndrome.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4714868/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4714868/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vijay-Kumar, Matam -- Aitken, Jesse D -- Carvalho, Frederic A -- Cullender, Tyler C -- Mwangi, Simon -- Srinivasan, Shanthi -- Sitaraman, Shanthi V -- Knight, Rob -- Ley, Ruth E -- Gewirtz, Andrew T -- DK061417/DK/NIDDK NIH HHS/ -- DK06439/DK/NIDDK NIH HHS/ -- DK083275/DK/NIDDK NIH HHS/ -- K01 DK083275/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Apr 9;328(5975):228-31. doi: 10.1126/science.1179721. Epub 2010 Mar 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Emory University, Atlanta, GA 30322, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20203013" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Bacterial Physiological Phenomena ; Blood Glucose/analysis ; Body Fat Distribution ; Body Weight ; Caloric Restriction ; Dietary Fats/administration & dosage ; Female ; Germ-Free Life ; Hyperphagia/etiology ; *Immunity, Innate ; Insulin Resistance ; Intestinal Mucosa/immunology ; Intestines/*microbiology ; Male ; Metabolic Syndrome X/*etiology/immunology/microbiology ; Mice ; Mice, Knockout ; Obesity/etiology/immunology/microbiology/prevention & control ; Toll-Like Receptor 5/deficiency/genetics/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Viral infection. Prevention and cure of rotavirus infection via TLR5/NLRC4-mediated production of IL-22 and IL-18 (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-11-15
    Description: Activators of innate immunity may have the potential to combat a broad range of infectious agents. We report that treatment with bacterial flagellin prevented rotavirus (RV) infection in mice and cured chronically RV-infected mice. Protection was independent of adaptive immunity and interferon (IFN, type I and II) and required flagellin receptors Toll-like receptor 5 (TLR5) and NOD-like receptor C4 (NLRC4). Flagellin-induced activation of TLR5 on dendritic cells elicited production of the cytokine interleukin-22 (IL-22), which induced a protective gene expression program in intestinal epithelial cells. Flagellin also induced NLRC4-dependent production of IL-18 and immediate elimination of RV-infected cells. Administration of IL-22 and IL-18 to mice fully recapitulated the capacity of flagellin to prevent or eliminate RV infection and thus holds promise as a broad-spectrum antiviral agent.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Benyue -- Chassaing, Benoit -- Shi, Zhenda -- Uchiyama, Robin -- Zhang, Zhan -- Denning, Timothy L -- Crawford, Sue E -- Pruijssers, Andrea J -- Iskarpatyoti, Jason A -- Estes, Mary K -- Dermody, Terence S -- Ouyang, Wenjun -- Williams, Ifor R -- Vijay-Kumar, Matam -- Gewirtz, Andrew T -- AI038296/AI/NIAID NIH HHS/ -- AI080656/AI/NIAID NIH HHS/ -- AI107943/AI/NIAID NIH HHS/ -- DK061417/DK/NIDDK NIH HHS/ -- DK064730/DK/NIDDK NIH HHS/ -- DK56338/DK/NIDDK NIH HHS/ -- R01 AI038296/AI/NIAID NIH HHS/ -- R37 AI038296/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2014 Nov 14;346(6211):861-5. doi: 10.1126/science.1256999.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Inflammation, Immunity and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA, USA. ; Center for Inflammation, Immunity and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA, USA. Department of Pathology, Emory University School of Medicine, Atlanta, GA, USA. ; Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX, USA. ; Elizabeth B. Lamb Center for Pediatric Research, Vanderbilt University School of Medicine, Nashville, TN, USA. ; Elizabeth B. Lamb Center for Pediatric Research, Vanderbilt University School of Medicine, Nashville, TN, USA. Departments of Pediatrics, Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, TN, USA. ; Department of Immunology, Genentech, South San Francisco, CA, USA. ; Department of Pathology, Emory University School of Medicine, Atlanta, GA, USA. ; Department of Nutritional Sciences and Medicine, Pennsylvania State University, University Park, PA 16802, USA. ; Center for Inflammation, Immunity and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA, USA. Department of Pathology, Emory University School of Medicine, Atlanta, GA, USA. agewirtz@gsu.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25395539" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Diarrhea/immunology/therapy/virology ; Disease Models, Animal ; Feces/virology ; Flagellin/*administration & dosage/immunology ; Homeodomain Proteins/genetics ; *Immunity, Innate ; Interleukin-18/administration & dosage/genetics/*immunology ; Interleukins/administration & dosage/genetics/*immunology ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Mutation ; Rotavirus Infections/immunology/*prevention & control/therapy ; Toll-Like Receptor 5/genetics/*physiology ; Virus Shedding
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Dietary emulsifiers impact the mouse gut microbiota promoting colitis and metabolic syndrome (2015)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2015-03-04
    Description: The intestinal tract is inhabited by a large and diverse community of microbes collectively referred to as the gut microbiota. While the gut microbiota provides important benefits to its host, especially in metabolism and immune development, disturbance of the microbiota-host relationship is associated with numerous chronic inflammatory diseases, including inflammatory bowel disease and the group of obesity-associated diseases collectively referred to as metabolic syndrome. A primary means by which the intestine is protected from its microbiota is via multi-layered mucus structures that cover the intestinal surface, thereby allowing the vast majority of gut bacteria to be kept at a safe distance from epithelial cells that line the intestine. Thus, agents that disrupt mucus-bacterial interactions might have the potential to promote diseases associated with gut inflammation. Consequently, it has been hypothesized that emulsifiers, detergent-like molecules that are a ubiquitous component of processed foods and that can increase bacterial translocation across epithelia in vitro, might be promoting the increase in inflammatory bowel disease observed since the mid-twentieth century. Here we report that, in mice, relatively low concentrations of two commonly used emulsifiers, namely carboxymethylcellulose and polysorbate-80, induced low-grade inflammation and obesity/metabolic syndrome in wild-type hosts and promoted robust colitis in mice predisposed to this disorder. Emulsifier-induced metabolic syndrome was associated with microbiota encroachment, altered species composition and increased pro-inflammatory potential. Use of germ-free mice and faecal transplants indicated that such changes in microbiota were necessary and sufficient for both low-grade inflammation and metabolic syndrome. These results support the emerging concept that perturbed host-microbiota interactions resulting in low-grade inflammation can promote adiposity and its associated metabolic effects. Moreover, they suggest that the broad use of emulsifying agents might be contributing to an increased societal incidence of obesity/metabolic syndrome and other chronic inflammatory diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chassaing, Benoit -- Koren, Omry -- Goodrich, Julia K -- Poole, Angela C -- Srinivasan, Shanthi -- Ley, Ruth E -- Gewirtz, Andrew T -- DK083890/DK/NIDDK NIH HHS/ -- DK099071/DK/NIDDK NIH HHS/ -- R01 DK083890/DK/NIDDK NIH HHS/ -- R01 DK099071/DK/NIDDK NIH HHS/ -- England -- Nature. 2015 Mar 5;519(7541):92-6. doi: 10.1038/nature14232. Epub 2015 Feb 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Inflammation, Immunity and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, Georgia 30303, USA. ; Faculty of Medicine, Bar Ilan University, Safed, 13115, Israel. ; Department of Molecular Biology and Genetics, Cornell University, Ithaca, New York 14853, USA. ; Digestive Diseases Division, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia 30322, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25731162" target="_blank"〉PubMed〈/a〉
    Keywords: Adiposity/drug effects ; Animals ; Carboxymethylcellulose Sodium/administration & dosage/adverse effects ; Colitis/*chemically induced/*microbiology/pathology ; Diet/*adverse effects ; Emulsifying Agents/administration & dosage/*adverse effects ; Feces/microbiology ; Female ; Gastrointestinal Tract/*drug effects/*microbiology/pathology ; Germ-Free Life ; Inflammation/chemically induced/microbiology/pathology ; Intestinal Mucosa/drug effects/microbiology/pathology ; Male ; Metabolic Syndrome X/*chemically induced/*microbiology/pathology ; Mice ; Microbiota/drug effects ; Obesity/chemically induced/microbiology/pathology ; Polysorbates/administration & dosage/adverse effects
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 5
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    Corrigendum: Dietary emulsifiers impact the mouse gut microbiota promoting colitis and metabolic syndrome (2016)
    Nature Publishing Group (NPG)
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    Publication Date: 2016-05-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chassaing, Benoit -- Koren, Omry -- Goodrich, Julia K -- Poole, Angela C -- Srinivasan, Shanthi -- Ley, Ruth E -- Gewirtz, Andrew T -- Nature. 2016 May 4. doi: 10.1038/nature18000.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27144359" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 6
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    From The Cover: Identification of hepoxilin A3 in inflammatory events: A required role in neutrophil migration across intestinal epithelia (2004)
    National Academy of Sciences
    Details
    Publication Date: 2004-05-03
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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