Activation and regulation of NFκB during acute inflammation

During the acute inflammatory response,there its induction of a mediator cascade which functions to activate residential macrophages and recruit blood leukocytes to the site of the inflammatory insult. Dysregulation of this process can cause an exaggerated inflammatory response and lead to tissue injury. Recent studies have focused on the transcription factor NF kappa B, which controls the gene expression of many pro-inflammatory mediators. Under normal conditions, NF kappa B is retained in the cytosol by inhibitory proteins of the I kappa B family. In response to an inflammatory insult, I kappa B proteins are degraded and the free NF kappa B complex translocates to the nucleus where it initiates gene transcription. An understanding of the in vivo mechanisms leading to the activation of NF kappa B, and the regulatory mechanisms that exist to limit this activation, may lead to the development of novel new therapeutic options for inflammatory injury. In this review we will discuss the current knowledge of the role of NF kappa B in the development of acute inflammation, as well as the regulatory mechanisms that exist to prevent the activation of NF kappa B and resolve inflammatory tissue injury.