Does Decreased c-KIT Expression in Myenteric Interstitial Cells of Cajal Cause Decreased Spontaneous Contraction in Murine Proximal Colon?

Abstract

In the current issue of the Journal of Neurogastroenterology and Motility, an article entitled "Alterations of colonic contractility in an IL-10 knockout mouse model of inflammatory bowel disease" demonstrated that interleukin-10 (IL-10) knockout mice exhibited altered colonic contractility and damaged interstitial cells of Cajal (ICC) networks. It also exhibited a decreased cholinergic response, caused by lowered expression of muscarinic receptors in the proximal colon and decreased neuronal nitric oxide synthase expression in both proximal and distal colon. For the past decades, more than 60 different animal models have been applied to study inflammatory bowel disease (IBD), which can be divided into chemically induced, cell-transfer, congenital mutant and genetically engineered models.2 Genetic techniques such as inducible knockout and knockin systems make it possible to characterize the mechanisms that are dysregulated in IBD.2 Up to date, most IBD studies have focused on mucosal inflammation and healing or related pathomechanisms. 3 The lesions in most IBD models are limited to the mucosa or submucosa area and the observed lesions resemble those found in colitis; as such, no existing models satisfactorily recapitulate the human disease. 4The animal model used in this study, however, showed inflammatory cell infiltration in all colonic layers (including the muscular layer) and exhibited lesions similar to those found in Crohn's disease. 1 This paper does take a novel approach by studying changes in smooth muscle and motility in an immunodeficiency model. The findings from this paper suggest that IL-10