Abstract
The systemic inflammatory response syndrome (SIRS) is a leading cause of morbidity and mortality in adults and children. Various proinflammatory mediators have been implicated in the pathogenesis of SIRS; however, their mechanisms of action are poorly defined. Recent evidence suggests that nitric oxide (NO) plays a regulatory role in gut barrier function. Sustained upregulation of NO production in the intestine can lead to intestinal epithelial injury through the formation of peroxynitrite. Peroxynitrite can nitrate mitochondrial proteins and inhibit cellular respiration. The resultant changes in mitochondrial function lead to activation of the caspase cascade, subsequent DNA fragmentation, and enterocyte apoptosis. Enterocyte apoptosis results in a transient "bare area" in the intestinal epithelium where bacteria can attach and then penetrate the lamina propria. Bacteria that successfully escape the immune system may in turn incite a systemic inflammatory response.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
