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Abstract
Background : Inhibition of NF- s B activation has been suggested as an anti-inflammatory treatment strategy in inflammatory bowel disease (IBD). However, NF- s B regulated genes like inducible nitric oxide synthase (iNOS) are also involved in cell survival mechanisms. Methods : Review of the literature on NF- s B activation and iNOS induction in IBD. Results : In patients with IBD the mucosal immune response is derailed. The nuclear transcription factor NF- s B is a key regulator of the inducible expression of many genes involved in immune and inflammatory responses in the gut. Stimuli like oxidative stress, cytokines (IL-1, IL-6, TNF- α ), bacteria and viruses can release NF- s B from their inactive cytoplasmatic form to the nucleus. Drugs like corticosteroids, sulphasalazine, mesalazine and inhibitory cytokines (e.g. IL-10, IL-11) can prevent the activation of NF- s B. New, more potent and selective treatment strategies with antisense p65, proteasome inhibitors and viral I s B α expression vectors aim at the prevention of NF- s B activation in mucosal macrophages and T lymphocytes. However, NF- s B regulated genes are also involved in survival responses of epithelial cells. For example, inhibition of the NF- s B mediated induction of iNOS in epithelial cells could block important anti-apoptotic and anti-microbial survival mechanisms. Nitric oxide may also serve in a negative feedback loop to antagonize prolonged activation of NF- s B, thereby limiting chronic inflammation. Conclusion : Luminal donation of nitric oxide could block NF- s B activation. Selective inhibition of NF- s B activation in inflammatory cells could be a treatment option in IBD.