Although cautious to point out that the present study derives from a well-differentiated, but transformed goblet cell line, Professor Gaskins said that "the data implicate biosynthesis of sulfomucins as a potential therapeutic target for the restoration of barrier function in chronic intestinal inflammatory disorders. Recent studies provide strong evidence that both ulcerative colitis (UC) and Crohn's disease (CD), the two primary types of IBD, result from multifactorial interactions among genetic, environmental and immunological factors that lead to a dysregulation of the innate immune response to the intestinal microbiota in genetically predisposed individuals."
The results with TNF are of particular interest because of its association with IBD and the alterations in mucin sulfation seen with active IBD. As IBD is characterized by dysregulated immune responsiveness, it may be that individuals with IBD fail to respond appropriately to TNF and, hence, fail to increase the production of sulfomucins. However, much additional work will be needed to better understand the mechanisms by which flagellin, IL-13, and TNF enhance expression of specific sulfotransferases and sulfomucin production.
Dr. Steve Goodman, Editor-in-Chief of Experimental Biology and Medicine said "Crohn's disease and ulcerative colitis (UC), the two primary types of inflammatory bowel disease (IBD), afflict 0.1-0.5% of individuals in Western countries with approximately 1 million Americans suffering from the disease at a cost of over $2 billion. This impressive study by Gaskins and colleagues identifies sulfomucins as potential targets for future therapies for chronic intestinal inflammatory disorders"
|Contact: Dr. H. Rex Gaskins|
Society for Experimental Biology and Medicine