Literature DB >> 10667419

Decreased expression of protectin (CD59) in gut epithelium in ulcerative colitis and Crohn's disease.

T Scheinin1, T Böhling, L Halme, S Kontiainen, L Bjørge, S Meri.   

Abstract

Without adequate protection, the cells of the human body would be susceptible to destruction by the complement system. The main defense against complement lysis is a molecule called protectin (CD59) that is widely distributed in human tissues. Because the complement system has been suggested to be involved in the pathogenesis of inflammatory bowel diseases, we examined the expression of protectin in the colonic epithelium of patients with ulcerative colitis or Crohn's disease and controls. Colorectal specimens from 6 patients with ulcerative colitis, 8 patients with Crohn's disease, and 4 controls were obtained from surgical resections. Frozen sections of the specimens were immunostained for protectin using the Bric 229 monoclonal antibody. The expression of protectin was found to be decreased in the epithelium of patients with ulcerative colitis. In patients with Crohn's disease, the epithelial expression of protectin was decreased in diseased areas of gut while the expression did not significantly differ from that in controls in macroscopically normal areas. There was no difference in the expression of protectin on vascular endothelium, mononuclear cells, or smooth muscle. The reduction in epithelial expression of protectin in patients with ulcerative colitis or Crohn's disease may render epithelial cells vulnerable to complement lysis and lead to the destruction of gut epithelium as seen typically in these diseases.

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Year:  1999        PMID: 10667419     DOI: 10.1016/s0046-8177(99)90163-6

Source DB:  PubMed          Journal:  Hum Pathol        ISSN: 0046-8177            Impact factor:   3.466


  11 in total

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2.  Regulation of the alternative pathway of complement modulates injury and immunity in a chronic model of dextran sulphate sodium-induced colitis.

Authors:  M Elvington; J Schepp-Berglind; S Tomlinson
Journal:  Clin Exp Immunol       Date:  2015-03       Impact factor: 4.330

3.  Complement activation promotes colitis-associated carcinogenesis through activating intestinal IL-1β/IL-17A axis.

Authors:  C Ning; Y-Y Li; Y Wang; G-C Han; R-X Wang; H Xiao; X-Y Li; C-M Hou; Y-F Ma; D-S Sheng; B-F Shen; J-N Feng; R-F Guo; Y Li; G-J Chen
Journal:  Mucosal Immunol       Date:  2015-03-04       Impact factor: 7.313

4.  Activation and Costimulation of Intestinal T Cells: Independent and Collaborative Involvement of CD43, OX40, and Ly-6C.

Authors:  Dina Montufar-Solis; John R Klein
Journal:  Curr Immunol Rev       Date:  2005-01

5.  A novel protocol allowing oral delivery of a protein complement inhibitor that subsequently targets to inflamed colon mucosa and ameliorates murine colitis.

Authors:  M Elvington; P Blichmann; F Qiao; M Scheiber; C Wadsworth; I Luzinov; J Lucero; A Vertegel; S Tomlinson
Journal:  Clin Exp Immunol       Date:  2014-08       Impact factor: 4.330

6.  Complement-dependent injury and protection in a murine model of acute dextran sulfate sodium-induced colitis.

Authors:  Jennifer Schepp-Berglind; Carl Atkinson; Michelle Elvington; Fei Qiao; Peter Mannon; Stephen Tomlinson
Journal:  J Immunol       Date:  2012-05-07       Impact factor: 5.422

7.  Complement activation capacity in plasma before and during high-dose prednisolone treatment and tapering in exacerbations of Crohn's disease and ulcerative colitis.

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Journal:  BMC Gastroenterol       Date:  2005-09-22       Impact factor: 3.067

8.  The complement anaphylatoxin C3a receptor (C3aR) contributes to the inflammatory response in dextran sulfate sodium (DSS)-induced colitis in mice.

Authors:  Elisabeth Wende; Robert Laudeley; André Bleich; Eva Bleich; Rick A Wetsel; Silke Glage; Andreas Klos
Journal:  PLoS One       Date:  2013-04-26       Impact factor: 3.240

9.  Differential gene expression in disease: a comparison between high-throughput studies and the literature.

Authors:  Raul Rodriguez-Esteban; Xiaoyu Jiang
Journal:  BMC Med Genomics       Date:  2017-10-11       Impact factor: 3.063

Review 10.  A Protective and Pathogenic Role for Complement During Acute Toxoplasma gondii Infection.

Authors:  Patricia M Sikorski; Alessandra G Commodaro; Michael E Grigg
Journal:  Front Cell Infect Microbiol       Date:  2021-02-22       Impact factor: 5.293

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