Welcome to the Blennerhassett Lab
We examine the effects of inflammation on the nerve-smooth muscle relationship of the intestine, which important in normal physiology, but may be a novel aspect of the disease process in inflammatory bowel disease (IBD), which is a serious medical problem for an increasing number of Canadians. For those with Crohn’s Disease (a type of IBD), the entire intestinal wall is inflamed and becomes increasingly thickened, which may cause stricturing and require surgery. My research looks at the cause of stricture formation and ways to prevent or reverse this process. For this, we use human tissue obtained by surgery, as well as an animal model that shows good parallel to the human disease. Our recent work has shown that the deeper layers of the intestine containing the enteric neurons and smooth muscle can be irreversibly affected by inflammation. For example, the smooth muscle grows, and the nervous system has to expand in parallel, but is also damaged. We propose that the growth of smooth muscle also means the release of a factor (Glial-derived neurotrophic factor or GDNF) that helps the neurons to survive and extend axons to innervate their target tissue (the smooth muscle). Furthermore, if the smooth muscle keeps growing (and it does in continued inflammation), it seems to lose this ability, and also changes its nature in a way that keeps it proliferating even more.
The cover image, by M. G. Blennerhassett et al., is based on the Original Article Analgesia and mouse strain influence neuromuscular plasticity in inflamed intestine, DOI: 10.1111/nmo.13097.