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Semin Immunol. 2018 Jun;37:66-73. doi: 10.1016/j.smim.2018.02.008. Epub 2018 Feb 24.

The intestinal complement system in inflammatory bowel disease: Shaping intestinal barrier function.

Author information

1
Institute of Nutritional Medicine, Molecular Gastroenterology, University Hospital Schleswig-Holstein, Campus Lübeck, Ratzeburger Allee 160, 23538 Lübeck, Germany; 1st Department of Medicine, Section of Nutritional Medicine, University Hospital Schleswig-Holstein, Campus Lübeck, Ratzeburger Allee 160, 23538 Lübeck, Germany.
2
Institute for Systemic Inflammation Research, University of Lübeck, Ratzeburger Allee 160, 23538 Lübeck, Germany; Division of Transplant Immunology and Mucosal Biology, Medical Research Council Centre for Transplantation, King's College London, Guy's Hospital, Great Maze Pond, London SE1 9RT, UK; Laboratory of Molecular Immunology and the Immunology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA.
3
Institute of Nutritional Medicine, Molecular Gastroenterology, University Hospital Schleswig-Holstein, Campus Lübeck, Ratzeburger Allee 160, 23538 Lübeck, Germany. Electronic address: Stefanie.derer@uksh.de.

Abstract

The complement system is part of innate sensor and effector systems such as the Toll-like receptors (TLRs). It recognizes and quickly systemically and/or locally respond to microbial-associated molecular patterns (MAMPs) with a tailored defense reaction. MAMP recognition by intestinal epithelial cells (IECs) and appropriate immune responses are of major importance for the maintenance of intestinal barrier function. Enterocytes highly express various complement components that are suggested to be pivotal for proper IEC function. Appropriate activation of the intestinal complement system seems to play an important role in the resolution of chronic intestinal inflammation, while over-activation and/or dysregulation may worsen intestinal inflammation. Mice deficient for single complement components suffer from enhanced intestinal inflammation mimicking the phenotype of patients with chronic inflammatory bowel disease (IBD) such as Crohn's disease (CD) or ulcerative colitis (UC). However, the mechanisms leading to complement expression in IECs seem to differ markedly between UC and CD patients. Hence, how IECs, intestinal bacteria and epithelial cell expressed complement components interact in the course of IBD still remains to be mostly elucidated to define potential unique patterns contributing to the distinct subtypes of intestinal inflammation observed in CD and UC.

KEYWORDS:

Chronic inflammatory bowel disease; Complement system; Crohn’s disease; Intestinal epithelial cells; Ulcerative colitis

PMID:
29486961
DOI:
10.1016/j.smim.2018.02.008
[Indexed for MEDLINE]

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