Inflammatory bowel disease pathophysiology

Characterize the pathophysiologic mechanisms underlying inflammatory bowel disease (IBD). 

There is evidence that induction of iNOS in a number of pathophysiological conditions is part of an uncontrolled and deleterious immune activation, for inhibition of NOS exerts protective effects in these conditions. The role of enhanced formation of NO in the circulatory failure associated with endotoxic, hemorrhagic, and other types of shock has recently been discussed elsewhere (Nussler and Billiar, 1993 Thiemermann, 1994 Szabo and Thiemermann, 1994). Increased levels of nitrite in the serum and synovial samples from patients with rheumatic arthritis and osteoarthritis have been reported this is likely to be due to the induction of iNOS at inflammatory sites (Farrell et al., 1992). Inhibition of iNOS attenuates acute and chronic inflammatory reactions as well as some of the pathophysiological manifestations of arthritis in various experimental models (lalenti et al., 1992 Lippe etal., 1993 McCartney-Francis a/., 1993 Stefanovic-Racic c a/., 1993). iNOS can also be expressed in various chronic inflammatory reactions of the central nervous system. Enhanced formation of NO derived form iNOS has also been implicated in the pathophysiology of chronic inflammatory bowel disease (Yamada et al., 1962 Middleton et al., 1993 Miller et al.,... 

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