Abstract
Neutrophil accumulation within epithelial crypts and in the intestinal mucosa directly correlates with clinical disease activity and epithelial injury in ulcerative colitis (UC). Current advances have defined the mechanisms by which neutrophils are activated or migrate across mucosal epithelia. A better understanding of this process will likely provide new insights into novel treatment strategies for UC. Especially, activated neutrophils produce reactive oxygen and nitrogen species within intestinal mucosa, which induce oxidative stress. In clinically, we have succeeded to develop a novel granulocytes adsorptive apheresis therapy for UC. In this article, we discuss current advances to define the role of neutrophils-dependent oxidative stress in UC.
