The role of intestinal epithelial Duox2 in mediating microbe – host interaction and maintains mucosal homeostasis

Seminar Details
Wednesday, January 11, 2017 - 9:00am to 10:00am


Helmut Grasberger, M.D.
Research Fellow, Division of Gastroenterology


5623 Med. Sci. II (Wheeler Seminar Room)

John Kao, M.D.

Dual oxidase 2 (DUOX2), a hydrogen-peroxide generator at the apical membrane of gastrointestinal epithelia, is upregulated in patients with inflammatory bowel disease (IBD) before the onset of inflammation, and mutation in DUOX2 but little is known about its effects. We recently showed that intestinal epithelial DUOX2 is induced by mucosal adherent bacteria (e.g., SFB) and mice deficient in DUOX had increased bacterial translocation and activated immune defense pathways indicating DUOX2 prevents bacterial translocation thus maintains mucosal homeostasis. We have extended these findings and showed how SFB induces DUOX2 with increased H2O2 production which alters bacterial colonization at the intestinal mucosa. We also found that DUOX2 could mediate host defense against pathogens independent of Th17/IL-22 pathway thus SFB-induced DUOX2 response is an important innate epithelial host defense needed to maintain mucosal homeostasis. 

Sponsored by the Host Microbiome Initiative