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Activation and Regulation of NFκB during Acute Inflammation
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Alex B. Lentsch
Published/Copyright:
June 1, 2005
Abstract
During the acute inflammatory response, there is 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 NFκB, which controls the gene expression of many pro-inflammatory mediators. Under normal conditions, NFκB is retained in the cytosol by inhibitory proteins of the IκB family. In response to an inflammatory insult, IκB proteins are degraded and the free NFκB complex translocates to the nucleus where it initiates gene transcription. An understanding of the in vivo mechanisms leading to the activation of NFκB, 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 NFκB in the development of acute inflammation, as well as the regulatory mechanisms that exist to prevent the activation of NFκB and resolve inflammatory tissue injury.
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Published Online: 2005-06-01
Published in Print: 1999-03-01
Copyright (c)1999 by Walter de Gruyter GmbH & Co. KG
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