IL-22 Upregulates Epithelial Claudin-2 to Drive Diarrhea and Enteric Pathogen Clearance
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CiNii Research
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- 資料種別
- 記事
- 著者標目
- 出版年月日等
- 2017-06
- 出版年(W3CDTF)
- 2017-06
- タイトル(掲載誌)
- Cell Host & Microbe
- 巻号年月日等(掲載誌)
- 21 6
- 掲載巻
- 21
- 掲載号
- 6
- 掲載ページ
- 671-681.e4
- 掲載年月日(W3CDTF)
- 2017-06
- ISSN(掲載誌)
- 19313128
- 出版事項(掲載誌)
- Elsevier BV
- 件名標目
- 対象利用者
- 一般
- 標準番号(その他)
- PMID : 28618266
- DOI
- 10.1016/j.chom.2017.05.009
- 作成日(W3CDTF)
- 2017-06-14
- 著作権情報
- https://www.elsevier.com/tdm/userlicense/1.0/https://www.elsevier.com/legal/tdmrep-licensehttp://www.elsevier.com/open-access/userlicense/1.0/
- 関連情報(URI)
- 参照
- Possible Involvement of the Mucosal Claudin Expression in the Healing of a Refractory Ileocecal Ulcer in a Patient with Crohn's Disease Successfully Treated with InfliximabFunctional landscape of mechanistic diversity in 27 claudin family members at tight junctionsInnate immune sensing of rotavirus by intestinal epithelial cells leads to diarrheaClaudin-2 upregulation enhances intestinal permeability, immune activation, dysbiosis, and mortality in sepsisDifferential dependence on microbiota of <scp>IL</scp>‐23/<scp>IL</scp>‐22‐dependent gene expression between the small‐ and large‐intestinal epitheliaDouble mutation of <i>claudin‐1</i> and <i>claudin‐3</i> causes alopecia in infant miceHigh-fat diet aggravates experimental autoimmune pancreatitis through the activation of type I interferon signaling pathwaysPartners in Leaky Gut Syndrome: Intestinal Dysbiosis and AutoimmunityInactivation of paracellular cation-selective claudin-2 channels attenuates immune-mediated experimental colitis in miceThe Claudins: From Tight Junctions to Biological SystemsInterleukin 22 Expands Transit-Amplifying Cells While Depleting Lgr5+ Stem Cells via Inhibition of Wnt and Notch SignalingClaudin-3 regulates bile canalicular paracellular barrier and cholesterol gallstone core formation in miceClinical importance of IL-22 cascade in IBD
- 参照
- IL-22 suppresses the infection of porcine enteric coronaviruses and rotavirus by activating STAT3 signal pathwayAquaporin-3 mediates hydrogen peroxide-dependent responses to environmental stress in colonic epitheliaClaudin‐2‐mediated cation and water transport share a common poreInterleukin-13 Receptor α1-Dependent Responses in the Intestine Are Critical to Parasite ClearanceComplementarity and redundancy of IL-22-producing innate lymphoid cellsEpithelial-intrinsic IKKα expression regulates group 3 innate lymphoid cell responses and antibacterial immunityTargeted colonic claudin-2 expression renders resistance to epithelial injury, induces immune suppression, and protects from colitisEpithelial IL-22RA1-Mediated Fucosylation Promotes Intestinal Colonization Resistance to an Opportunistic PathogenSeparation of Intact Intestinal Epithelium from MesenchymeSTAT6 Deficiency Ameliorates Severity of Oxazolone Colitis by Decreasing Expression of Claudin-2 and Th2-Inducing CytokinesLoss of Claudins 2 and 15 From Mice Causes Defects in Paracellular Na+ Flow and Nutrient Transport in Gut and Leads to Death from MalnutritionClaudin-2 Regulates Colorectal Inflammation via Myosin Light Chain Kinase-Dependent SignalingTh22 Cells Are an Important Source of IL-22 for Host Protection against Enteropathogenic BacteriaActivated fluid transport regulates bacterial-epithelial interactions and significantly shifts the murine colonic microbiomeLong-term Expansion of Epithelial Organoids From Human Colon, Adenoma, Adenocarcinoma, and Barrett's EpitheliumPolyethylene glycol diminishes pathological effects of<i>Citrobacter rodentium</i>infection by blocking bacterial attachment to the colonic epitheliaInterleukin-6 (IL-6) Regulates Claudin-2 Expression and Tight Junction Permeability in Intestinal EpitheliumOccludin S408 phosphorylation regulates tight junction protein interactions and barrier functionEpithelial Myosin Light Chain Kinase Activation Induces Mucosal Interleukin-13 Expression to Alter Tight Junction Ion SelectivityA Comprehensive Proteomic Analysis of the Type III Secretome of Citrobacter rodentiumIntestinal mucosal barrier function in health and diseasePhysiology and Function of the Tight JunctionSTAT3 links IL-22 signaling in intestinal epithelial cells to mucosal wound healingTNFα up-regulates claudin-2 expression in epithelial HT-29/B6 cells via phosphatidylinositol-3-kinase signalingInterleukin-22 mediates early host defense against attaching and effacing bacterial pathogensClaudin profiling in the mouse during postnatal intestinal development and along the gastrointestinal tract reveals complex expression patternsAttaching and effacing pathogen-induced tight junction disruption in vivoEpithelial myosin light chain kinase-dependent barrier dysfunction mediates T cell activation-induced diarrhea in vivoPhenotype analysis of aquaporin-8 null miceRegulatory Sequences of the Mouse Villin Gene That Efficiently Drive Transgenic Expression in Immature and Differentiated Epithelial Cells of Small and Large IntestinesAdverse Effect of Lomotil Therapy in ShigellosisA BACTERIOLOGICAL AND CLINICAL CONSIDERATION OF BACILLARY DYSENTERY IN ADULTS AND CHILDREN
- 連携機関・データベース
- 国立情報学研究所 : CiNii Research
- 提供元機関・データベース
- Crossref科学研究費助成事業データベース科学研究費助成事業データベース学術機関リポジトリデータベース学術機関リポジトリデータベースCrossrefCrossrefCrossrefCrossrefCrossrefCrossrefCrossrefCrossrefCrossrefCrossrefCrossrefCrossrefCrossref
- 要約等
- <p>Diarrhea is a host response to enteric pathogens, but its impact on pathogenesis remains poorly defined. By infecting mice with the attaching and effacing bacteria Citrobacter rodentium, we defined the mechanisms and contributions of diarrhea and intestinal barrier loss to host defense. Increased permeability occurred within 2 days of infection and coincided with IL-22-dependent upregulation of the epithelial tight junction protein claudin-2. Permeability increases were limited to small molecules, as expected for the paracellular water and Na<sup>+</sup> channel formed by claudin-2. Relative to wild-type, claudin-2-deficient mice experienced severe disease, including increased mucosal colonization by C. rodentium, prolonged pathogen shedding, exaggerated cytokine responses, and greater tissue injury. Conversely, transgenic claudin-2 overexpression reduced disease severity. Chemically induced osmotic diarrhea reduced colitis severity and C. rodentium burden in claudin-2-deficient, but not transgenic, mice, demonstrating that claudin-2-mediated protection is the result of enhanced water efflux. Thus, IL-22-induced claudin-2 upregulation drives diarrhea and pathogen clearance.</p>
- DOI
- 10.1016/j.chom.2017.05.009
- 異版(DOI)
- 10.1016/j.chom.2017.05.009
- 連携機関・データベース
- 国立情報学研究所 : 学術機関リポジトリデータベース(IRDB)(機関リポジトリ)
- 提供元機関・データベース
- 帝京大学 : 帝京大学研究・教育リポジトリ