Although the inflammatory bowel diseases – ulcerative colitis and Crohn’s disease – have distinct patterns of injury and inflammation, the existing therapies are quite similar and no therapies specifically target the Th2 immune response activated in ulcerative colitis.
The signaling molecule IL-13 (a key Th2 cytokine) has been implicated in the pathogenesis of the disease, but no group has demonstrated evidence of increased IL-13 signaling in colon tissues of patients with the disease.
Michael Rosen, assistant professor of pediatrics, and colleagues now show that STAT6, the key transcription factor activated by IL-13, is activated in colon tissue from pediatric patients recently diagnosed with ulcerative colitis.
In cell experiments, they found that STAT6 is involved in IL-13-induced epithelial cell death and barrier disruption, and that blocking STAT6 with the FDA-approved histone deacetylase inhibitor suberoylanilde hydroxamic acid (SAHA) inhibits these effects.
Sourece: Vanderbilt University