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Inflammatory cues modulate goblet cell products important for intestinal barrier function
Date:12/2/2011

In a paper published in the December 2011 issue of Experimental Biology and Medicine, a team of scientists at the University of Illinois, Urbana-Champaign led by Rex Gaskins, PhD have demonstrated that both microbial and host inflammatory factors modulate sulfomucin production in a human cell line, LS174T, that models intestinal goblet cells.

Sulfomucins, one of two primary types of acidomucins secreted by intestinal goblet cells, provide crucial protection to the intestinal mucosa. Therefore, it is not surprising that a loss of intestinal sulfomucins is associated with both inflammatory bowel disease (IBD) and colorectal cancer. However, the extent to which pathways involved in sulfomucin production are responsive to signals emanating directly from intestinal microbes or cues originating from host inflammatory cells is not known.

The research team at the University of Illinois compared the effects of bacterial flagellin to the mucogenic cytokine IL-13, and the proinflammatory cytokine TNF on expression of genes encoding the Golgi sulfotransferases involved in addition of sulfate groups to mucin precursors and sulfomucin production. They observed high induction of carbohydrate (N-acetyl-glucosamine 6-O) sulfotransferase 5 (CHST5) as early as 12 h after treatment with IL-13. Flagellin, IL-13 and TNF all, on the other hand, induced expression of the other sulfotransferase galactose-3-O-sulfotransferase 2 (GAL3ST2). The observed induction of sulfotransferases was consistent with increased sulfomucin production by LS174T cells in response to IL-13 and flagellin, indicating that sulfotransferases and sulfomucin synthesis can be differentially modulated by particular inflammatory signals.

Galactose-3-O-sulfotransferase 2 is thought to be the sulfotransferase responsible for sulfate addition to the C-3 position of galactose in human colonic mucins. On the other hand, CHST5 is the most likely candidate for sulfation of the C-
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Contact: Dr. H. Rex Gaskins
hgaskins@illinois.edu
217-444-3165
Society for Experimental Biology and Medicine
Source:Eurekalert

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