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Role of interleukin 6 in a murine model of Crohn’s ileitis: are cytokine/anticytokine strategies the future for IBD therapies?
  1. T T Pizarro,
  2. S A De La Rue,
  3. F Cominelli
  1. Digestive Health Center of Excellence, University of Virginia Health System, Charlottesville, VA, 22908, USA
  1. Correspondence to:
    Dr F Cominelli
    University of Virginia Health System, Digestive Health Center of Excellence, PO Box 800708, Charlottesville, Virginia, USA 22908; FC4Q{at}virginia.edu

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Although the precise causes of inflammatory bowel disease (IBD) have yet to be discovered, important therapeutic advances have resulted from the manipulation of cytokine function(s) using anticytokine/cytokine therapies, such as targeting of tumour necrosis factor. We discuss the future of this area of investigation in the context of preclinical experimentation using animal models of IBD. In particular, we pinpoint the roles played by interleukin 6 and its intracellular signalling pathways in the SAMP1/Yit murine model of Crohn’s-like ileitis.

Oer the past several years, a variety of animal models of inflammatory bowel disease (IBD) have been developed and investigated, with the ultimate goal of understanding the causes of Crohn’s disease (CD) and ulcerative colitis (UC).1,2 Unfortunately, thus far no single animal model recapitulates all of the pathogenic and clinical features of human IBD, which has impeded our progress towards an understanding of the precise causes of these devastating diseases. Nevertheless, each animal model has provided us with a unique opportunity to advance our understanding of the mechanisms underlying initiation and perpetuation of chronic intestinal inflammation. This has allowed identification of novel targets in the disease process for potential therapeutic intervention. For instance, the explosion in the number of animal models of colitis based on gene deletion or overexpression has underlined the importance of cytokine gene products in gut immune regulation.3 Perhaps one of the best examples in this category is the interleukin (IL)-10 deficient mouse, which develops chronic enteritis, the characteristics of which are similar to human IBD.4 Despite the fact that no genetic or immunological abnormalities of the IL-10 pathway have been demonstrated in patients with IBD to date, this model has facilitated the development of therapeutic strategies based on administration of anti-inflammatory cytokines5 or delivery of regulatory T cells with anti-inflammatory activities.6

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