NEW YORK (Reuters Health) - Direct delivery of an oligonucleotide that binds nuclear factor-kappa B (NFkB) ameliorates murine inflammatory bowel disease (IBD) and restores tissue homeostasis, researchers report in the April issue of Gut.

"The NFkB decoy for IBD," senior researcher Dr. Rolf O. Ehrhardt told Reuters Health, "has the potential to be used as a 'crossfunctional' drug for both ulcerative colitis and Crohn's disease."

Dr. Ehrhardt of Intermune, Inc. in Brisbane, California and colleagues note that NFkB is a key transcriptional regulator of IBD. With this is mind, the team developed a decoy oligonucleotide that specifically binds NFkB and blocks associated inflammatory mediators.

Apparently because of the stability of the agent and its chemistry, use of viral envelope-assisted delivery is not required.

In a mouse model of colitis, intracolonic administration of the decoy led to a dose-dependent reduction in disease severity and more rapid recovery of normal body weight.

Such treatment also led to considerable reductions in colitis pathology and tissue levels of several pro-inflammatory markers, including TNF-alpha, interleukin 6, and interleukin 1b. The team also found a rapid return to normal patterns of cell proliferation in the mucosal epithelium and smooth muscle cell layers.

Given these findings, concluded Dr. Ehrhardt, "the drug might not only suppress inflammation successfully, but also support mucosal repair mechanisms that are important for the maintenance of mucosal homeostasis."