Journal
JOURNAL OF CROHNS & COLITIS
Volume 10, Issue 12, Pages 1417-1427Publisher
OXFORD UNIV PRESS
DOI: 10.1093/ecco-jcc/jjw111
Keywords
Citrobacter rodentium; colitis; DSS
Categories
Funding
- Wellcome Trust [088683/Z/09/Z]
- United Kingdom Medical Research Council [G0902005]
- Wellcome Trust [088683/Z/09/Z] Funding Source: Wellcome Trust
- MRC [MR/L000261/1, G0902022, G0902005] Funding Source: UKRI
- Medical Research Council [MR/L000261/1, G0902022, G0902005] Funding Source: researchfish
- National Institute for Health Research [ACF-2008-18-011] Funding Source: researchfish
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Background and Aims: ADAM [A Disintegrin And Metalloproteinase] is a family of peptidase proteins which have diverse roles in tissue homeostasis and immunity. Here, we study ADAM-like DECysin-1 [ADAMDEC1] a unique member of the ADAM family. ADAMDEC1 expression is restricted to the macrophage/dendritic cell populations of the gastrointestinal tract and secondary lymphoid tissue. The biological function of ADAMDEC1 is unknown but it has been hypothesised to play a role in immunity. The identification of reduced ADAMDEC1 expression in Crohn's disease patients has provided evidence of a potential role in bowel inflammation. Methods: Adamdec1(-/-) mice were exposed to dextran sodium sulphate or infected orally with Citrobacter rodentium or Salmonella typhimurium. The clinical response was monitored. Results: The loss of Adamdec1 rendered mice more susceptible to the induction of bacterial and chemical induced colitis, as evidenced by increased neutrophil infiltration, greater IL-6 and IL-1 beta secretion, more weight loss and increased mortality. In the absence of Adamdec1, greater numbers of Citrobacter rodentium were found in the spleen, suggestive of a breakdown in mucosal immunity which resulted in bacteraemia. Conclusion: In summary, ADAMDEC1 protects the bowel from chemical and bacterial insults, failure of which may predispose to Crohn's disease.
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