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Receptor-Dependent Mechanisms of Cell Stimulation by Bacterial Endotoxin

Receptor-Dependent Mechanisms of Cell Stimulation by Bacterial Endotoxin In humans and experimental animals the presence of bacterial lipopolysaccha­ ride (endotoxin, LPS) signals the presence of gram-negative bacteria. Recogni­ tion of LPS triggers gene induction by myeloid and nonmyeloid lineage cells. These inducible genes encode proteins that include cytokines, adhesive proteins, and enzymes that produce low molecular weight proinflammatory mediators. Together the products of these inducible genes upregulate host defense systems that participate in eliminating the bacterial infection. Unfortunately, these same mediators contribute to a serious human disease known as septic shock. Consid­ erable progress has been made during the past decade in determining the sources, identities, and sequence of release of these mediators. In contrast, until recently, marked gaps in our knowledge existed regarding the identity of the LPS receptor and intracellular signaling pathways responsible for LPS-induced cell activation. The discovery in of a plasma protein termed LPS binding protein (LBP) led to the discovery of unanticipated mechanisms of LPS-induced cell activation. CD14 was found as a soluble serum protein or as a glycosylphosphatidylinositol (GPI)-anchored protein of myeloid lineage cells; it now occupies a key role in LPS-induced cell activation as we understand it today. Here we discuss how LBP enables LPS binding to CD14 and http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Annual Review of Immunology Annual Reviews

Receptor-Dependent Mechanisms of Cell Stimulation by Bacterial Endotoxin

Annual Review of Immunology , Volume 13 (1) – Apr 1, 1995

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Publisher
Annual Reviews
Copyright
Copyright 1995 Annual Reviews. All rights reserved
Subject
Review Articles
ISSN
0732-0582
eISSN
1545-3278
DOI
10.1146/annurev.iy.13.040195.002253
pmid
7542010
Publisher site
See Article on Publisher Site

Abstract

In humans and experimental animals the presence of bacterial lipopolysaccha­ ride (endotoxin, LPS) signals the presence of gram-negative bacteria. Recogni­ tion of LPS triggers gene induction by myeloid and nonmyeloid lineage cells. These inducible genes encode proteins that include cytokines, adhesive proteins, and enzymes that produce low molecular weight proinflammatory mediators. Together the products of these inducible genes upregulate host defense systems that participate in eliminating the bacterial infection. Unfortunately, these same mediators contribute to a serious human disease known as septic shock. Consid­ erable progress has been made during the past decade in determining the sources, identities, and sequence of release of these mediators. In contrast, until recently, marked gaps in our knowledge existed regarding the identity of the LPS receptor and intracellular signaling pathways responsible for LPS-induced cell activation. The discovery in of a plasma protein termed LPS binding protein (LBP) led to the discovery of unanticipated mechanisms of LPS-induced cell activation. CD14 was found as a soluble serum protein or as a glycosylphosphatidylinositol (GPI)-anchored protein of myeloid lineage cells; it now occupies a key role in LPS-induced cell activation as we understand it today. Here we discuss how LBP enables LPS binding to CD14 and

Journal

Annual Review of ImmunologyAnnual Reviews

Published: Apr 1, 1995

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