Ulcerative colitis and Crohn's disease are characterized by chronic intesti
nal inflammation. Intestinal bacteria initiate the activation of intestinal
inflammatory processes, which are mediated by proinflammatory cytokines an
d chemokines. In inflammatory bowel disease, intestinal inflammation is not
downregulated, in part due to defective or absent inhibitory processes. St
udies to date have demonstrated that IL-8, MCP-1, and ENA-78 are highly exp
ressed in the intestinal mucosa in areas of active Crohn's disease and ulce
rative colitis. Neutrophils and macrophages in the inflamed intestine synth
esize and secrete large amounts of chemokines in patients with inflammatory
bowel disease. Increased chemokine expression has also been observed in ep
ithelial cells, endothelial cells, and smooth muscle cells. Future trials o
f specific agents capable of inhibiting chemokine synthesis and secretion o
r blocking chemokine-chemokine receptor interaction will be important to st
udy in patients with ulcerative colitis and Crohn's disease.