本文へ移動
記事

IL-22 Upregulates Epithelial Claudin-2 to Drive Diarrhea and Enteric Pathogen Clearance

記事を表すアイコン

IL-22 Upregulates Epithelial Claudin-2 to Drive Diarrhea and Enteric Pathogen Clearance

資料種別
記事
著者
Pei-Yun Tsaiほか
出版者
Elsevier BV
出版年
2017-06
資料形態
デジタル
掲載誌名
Cell Host & Microbe 21 6
掲載ページ
p.671-681.e4
詳細を見る

資料詳細

要約等:

Diarrhea is a host response to enteric pathogens, but its impact on pathogenesis remains poorly defined. By infecting mice with the attaching and effa...

全国の図書館の所蔵

国立国会図書館サーチが連携している各図書館等から取得した所蔵情報を表示します。

所蔵館、利用可否等の詳細・最新状況は情報提供元の各館のサイト・データベースで直接ご確認ください。所蔵館から取寄せることが可能かなど、資料の利用方法は、ご自身が利用されるお近くの図書館へご相談ください。詳細は ヘルプ をご覧ください。

その他

  • 帝京大学研究・教育リポジトリ

    デジタル
    遷移先のサイトで、学術機関リポジトリデータベース(IRDB)(機関リポジトリ)が連携している機関・データベースの所蔵状況を確認できます。
  • CiNii Research

    検索サービス
    デジタル
    遷移先のサイトで、CiNii Researchが連携している機関・データベースの所蔵状況を確認できます。

書誌情報

この資料の詳細や典拠(同じ主題の資料を指すキーワード、著者名)等を確認できます。

デジタル

資料種別
記事
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
対象利用者
一般
標準番号(その他)
PMID : 28618266
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-license
http://www.elsevier.com/open-access/userlicense/1.0/
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 Infliximab
Functional landscape of mechanistic diversity in 27 claudin family members at tight junctions
Innate immune sensing of rotavirus by intestinal epithelial cells leads to diarrhea
Claudin-2 upregulation enhances intestinal permeability, immune activation, dysbiosis, and mortality in sepsis
Differential dependence on microbiota of <scp>IL</scp>‐23/<scp>IL</scp>‐22‐dependent gene expression between the small‐ and large‐intestinal epithelia
Double mutation of <i>claudin‐1</i> and <i>claudin‐3</i> causes alopecia in infant mice
High-fat diet aggravates experimental autoimmune pancreatitis through the activation of type I interferon signaling pathways
Partners in Leaky Gut Syndrome: Intestinal Dysbiosis and Autoimmunity
Inactivation of paracellular cation-selective claudin-2 channels attenuates immune-mediated experimental colitis in mice
The Claudins: From Tight Junctions to Biological Systems
Interleukin 22 Expands Transit-Amplifying Cells While Depleting Lgr5+ Stem Cells via Inhibition of Wnt and Notch Signaling
Claudin-3 regulates bile canalicular paracellular barrier and cholesterol gallstone core formation in mice
Clinical importance of IL-22 cascade in IBD
参照
IL-22 suppresses the infection of porcine enteric coronaviruses and rotavirus by activating STAT3 signal pathway
Aquaporin-3 mediates hydrogen peroxide-dependent responses to environmental stress in colonic epithelia
Claudin‐2‐mediated cation and water transport share a common pore
Interleukin-13 Receptor α1-Dependent Responses in the Intestine Are Critical to Parasite Clearance
Complementarity and redundancy of IL-22-producing innate lymphoid cells
Epithelial-intrinsic IKKα expression regulates group 3 innate lymphoid cell responses and antibacterial immunity
Targeted colonic claudin-2 expression renders resistance to epithelial injury, induces immune suppression, and protects from colitis
Epithelial IL-22RA1-Mediated Fucosylation Promotes Intestinal Colonization Resistance to an Opportunistic Pathogen
Separation of Intact Intestinal Epithelium from Mesenchyme
STAT6 Deficiency Ameliorates Severity of Oxazolone Colitis by Decreasing Expression of Claudin-2 and Th2-Inducing Cytokines
Loss of Claudins 2 and 15 From Mice Causes Defects in Paracellular Na+ Flow and Nutrient Transport in Gut and Leads to Death from Malnutrition
Claudin-2 Regulates Colorectal Inflammation via Myosin Light Chain Kinase-Dependent Signaling
Th22 Cells Are an Important Source of IL-22 for Host Protection against Enteropathogenic Bacteria
Activated fluid transport regulates bacterial-epithelial interactions and significantly shifts the murine colonic microbiome
Long-term Expansion of Epithelial Organoids From Human Colon, Adenoma, Adenocarcinoma, and Barrett's Epithelium
Polyethylene glycol diminishes pathological effects of<i>Citrobacter rodentium</i>infection by blocking bacterial attachment to the colonic epithelia
Interleukin-6 (IL-6) Regulates Claudin-2 Expression and Tight Junction Permeability in Intestinal Epithelium
Occludin S408 phosphorylation regulates tight junction protein interactions and barrier function
Epithelial Myosin Light Chain Kinase Activation Induces Mucosal Interleukin-13 Expression to Alter Tight Junction Ion Selectivity
A Comprehensive Proteomic Analysis of the Type III Secretome of Citrobacter rodentium
Intestinal mucosal barrier function in health and disease
Physiology and Function of the Tight Junction
STAT3 links IL-22 signaling in intestinal epithelial cells to mucosal wound healing
TNFα up-regulates claudin-2 expression in epithelial HT-29/B6 cells via phosphatidylinositol-3-kinase signaling
Interleukin-22 mediates early host defense against attaching and effacing bacterial pathogens
Claudin profiling in the mouse during postnatal intestinal development and along the gastrointestinal tract reveals complex expression patterns
Attaching and effacing pathogen-induced tight junction disruption in vivo
Epithelial myosin light chain kinase-dependent barrier dysfunction mediates T cell activation-induced diarrhea in vivo
Phenotype analysis of aquaporin-8 null mice
Regulatory Sequences of the Mouse Villin Gene That Efficiently Drive Transgenic Expression in Immature and Differentiated Epithelial Cells of Small and Large Intestines
Adverse Effect of Lomotil Therapy in Shigellosis
A 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

デジタル

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>
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