IMR Press / FBL / Volume 9 / Issue 2 / DOI: 10.2741/1304

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article

NF-κB action in sepsis: the innate immune system and the heart

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1 Department of Pharmacology and Cell Biophysics, 231 Albert Sabin Way ML0575, University of Cincinnati, Cincinnati, OH 45267-0575, USA
Academic Editor:Herbert B. Tanowitz
Front. Biosci. (Landmark Ed) 2004, 9(2), 1201–1217;
Published: 1 May 2004
(This article belongs to the Special Issue Infectious diseases of the myocardium)

Sepsis is the clinical syndrome that results from a host's inflammatory response to infection via activation of the innate immune system. This response involves a complex network of inflammatory mediators that is self-reinforcing. When this immune response progresses uncontrollably, it can ultimately result in cardiovascular collapse and death. This complex inflammatory response is comprised of multiple mediators including cytokines such as TNF-α and IL-1β, that are synthesized and secreted in response to signaling by receptors of the Toll-like receptor (TLR) family of pattern recognition receptors (PRR) that bind to pathogen associated molecules. A central downstream element of TLR-dependent signaling is the pleiotropic transcription factor NF-κB. NF-κB has been implicated in the regulation of multiple biological phenomena and disease states, including apoptosis, cell growth, stress response, innate immunity and septic shock. NF-κB-dependent genes are numerous and several have been implicated in the pathogenesis of sepsis and associated with cardiac dysfunction in sepsis. NF-κB activation occurs in multiple organs and cell types, and may be primarily protective in one tissue but injurious in another. Thus, a detailed understanding of the molecular basis of the pathophysiology of sepsis is needed in order to specifically block pro-inflammatory and pro-apoptotic signaling in the heart, while avoiding adverse effects in other organs.

Signal Transduction
Gene Expression
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