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by Leigh MacMillan | Friday, Apr. 25, 2014, 11:00 AM
Increased mucosal permeability (a “leaky” barrier) is a proposed contributor to inflammatory bowel diseases (IBD), such as ulcerative colitis and Crohn’s disease. Claudin-2 – part of the “tight junctions” that regulate epithelial permeability – is highly expressed in IBD and is believed to increase mucosal permeability and promote inflammation. However, its precise role in the regulation of mucosal inflammation remains unclear.
Now, Amar B. Singh, Ph.D., and colleagues have made the surprising discovery that transgenic mice overexpressing claudin-2 in the intestine are protected against experimental colitis, despite having a leaky gut. Claudin-2 transgenic mice did not have colitis-induced immune cell activation and contained non-responsive macrophages and more regulatory T-cells in their colon, compared to control mice. Claudin-2 mice were also protected from colitis-associated epithelial injury.
The findings, reported in Mucosal Immunology, reveal a critical role of claudin-2 in regulating intestinal homeostasis and barrier function, which then regulates mucosal immune activation and inflammation. The findings alter current understanding of the role of epithelial permeability and claudin-2 in intestinal homeostasis and immune regulation, and suggest new therapeutic opportunities for IBD.
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Health and Medicine, Reporter, Research Aliquots, Amar Singh, colitis, Crohn's disease, Department of Medicine, Department of Surgery, Department of Veterans Affairs, inflammatory bowel disease, Mucosal Immunology, NCI, NIDDK, NIH, Reporter April 25 2014, ulcerative colitis
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