| http://purl.uniprot.org/citations/22566568 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/22566568 | http://www.w3.org/2000/01/rdf-schema#comment | "Complement plays a key role in the pathophysiology of many inflammatory diseases, and in this study, we investigated the role of complement in the pathogenesis of inflammatory bowel disease. Compared to wild-type mice, mice deficient in C3 or factor B were protected from acute dextran sulfate sodium (DSS)-induced colitis. C1q/mannose-binding lectin (MBL) double-deficient mice, however, exhibited more severe colitis than wild-type mice. When mice were allowed to recover after DSS treatment, all C1q/MBL(-/-) mice died by day 2 of recovery period, and, surprisingly, all C3(-/-) and factor B(-/-) mice died by day 5. Serum endotoxin levels were significantly increased in complement-deficient mice prior to death, particularly in C1q/MBL(-/-) mice, and antibiotic treatment prevented the lethal effect of DSS in all complement-deficient mice. In contrast to complement deficiency, targeted complement inhibition with either complement receptor 2 (CR2)-Crry (blocks all pathways at C3 activation) or CR2-factor H (blocks alternative pathway) was highly protective at treating established acute colitis. Endotoxin levels remained low in complement-inhibited mice, and complement inhibition also reduced inflammatory cytokines, leukocyte infiltration, and tissue injury while improving wound repair and mucosal healing. CR2-factor H provided more effective protection than CR2-Crry. Thus, complement has both pathogenic and protective roles in acute DSS-induced colitis, and whereas the alternative pathway appears to play a key role in tissue inflammation and injury, the classical/lectin pathway provides important protection in terms of host defense and wound repair. Targeted inhibition of the alternative pathway may represent a therapeutic modality for treating acute phases of inflammatory bowel disease."xsd:string |
| http://purl.uniprot.org/citations/22566568 | http://purl.org/dc/terms/identifier | "doi:10.4049/jimmunol.1200553"xsd:string |
| http://purl.uniprot.org/citations/22566568 | http://purl.uniprot.org/core/author | "Atkinson C."xsd:string |
| http://purl.uniprot.org/citations/22566568 | http://purl.uniprot.org/core/author | "Tomlinson S."xsd:string |
| http://purl.uniprot.org/citations/22566568 | http://purl.uniprot.org/core/author | "Qiao F."xsd:string |
| http://purl.uniprot.org/citations/22566568 | http://purl.uniprot.org/core/author | "Mannon P."xsd:string |
| http://purl.uniprot.org/citations/22566568 | http://purl.uniprot.org/core/author | "Elvington M."xsd:string |
| http://purl.uniprot.org/citations/22566568 | http://purl.uniprot.org/core/author | "Schepp-Berglind J."xsd:string |
| http://purl.uniprot.org/citations/22566568 | http://purl.uniprot.org/core/date | "2012"xsd:gYear |
| http://purl.uniprot.org/citations/22566568 | http://purl.uniprot.org/core/name | "J Immunol"xsd:string |
| http://purl.uniprot.org/citations/22566568 | http://purl.uniprot.org/core/pages | "6309-6318"xsd:string |
| http://purl.uniprot.org/citations/22566568 | http://purl.uniprot.org/core/title | "Complement-dependent injury and protection in a murine model of acute dextran sulfate sodium-induced colitis."xsd:string |
| http://purl.uniprot.org/citations/22566568 | http://purl.uniprot.org/core/volume | "188"xsd:string |
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