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A biologically active substance produced by bacteria and consisting of lipopolysaccharide, a complex macromolecule containing a polysaccharide covalently linked to a unique lipid structure, termed lipid A. All gram-negative bacteria synthesize lipopolysaccharide, which is a major constituent of their outer cell membrane. One major function of lipopolysaccharide is to serve as a selectively permeable barrier for organic molecules in the external environment. Different types of gram-negative bacteria synthesize lipopolysaccharide with very different polysaccharide structures. The biological activity of endotoxic lipopolysaccharide resides almost entirely in the lipid A component. See Cell membranes, Lipid, Polysaccharide

When lipopolysaccharides are released from the outer membrane of the microorganism, significant host responses are initiated in humans and other mammals. It is generally accepted that lipopolysaccharides are among the most potent microbial products, known for their ability to induce pathophysiological changes, in particular fever and changes in circulating white blood cells. In humans as little as 4 nanograms of purified lipopolysaccharide per kilogram of body weight is sufficient to produce a rise in temperature of about 3.6°F (2°C) in several hours. This profound ability of the host to recognize endotoxin is thought to serve as an early warning system to signal the presence of gram-negative bacteria.

Unlike most microbial protein toxins (which have been termed bacterial exotoxins), endotoxin is unique in that its recognized mode of action does not result from direct damage to host cells and tissues. Rather, endotoxin stimulates cells of the immune system, particularly macrophages, and of the vascular system, primarily endothelial cells, to become activated and to synthesize and secrete a variety of effector molecules that cause an inflammatory response at the site of bacterial invasion. These mediator molecules promote the host response which results in elimination of the invading microbe. Thus, under these circumstances lipopolysaccharide is not a toxin at all, but serves an important function by helping to mobilize the host immune system to fight infection. See Cytokine, Immunology

Even though endotoxin stimulation of host cells is important to host defense against infection, overstimulation due to excess production of endotoxin can lead to serious consequences. Endotoxin-induced multiple-organ failure continues to be a major health problem, particularly in intensive care; it has been estimated that as many as 50,000 deaths annually occur in the United States as the result of endotoxin-induced shock.

Immunization of humans with endotoxin vaccines to protect against endotoxin shock has not been considered practical. Efforts to provide immunologic protection against endotoxin-related diseases have focused upon development of antibodies that recognize the conserved lipid A structure of endotoxin as a means of passive protection against the lethal effects of this microbial product. See Bacteria, Medical bacteriology, Vaccination

McGraw-Hill Concise Encyclopedia of Bioscience. © 2002 by The McGraw-Hill Companies, Inc.


A biologically active substance produced by gram-negative bacteria and consisting of lipopolysaccharide, a complex macromolecule containing a polysaccharide covalently linked to a unique lipid structure, termed lipid A.
McGraw-Hill Dictionary of Scientific & Technical Terms, 6E, Copyright © 2003 by The McGraw-Hill Companies, Inc.
References in periodicals archive ?
Shi, "The opioid antagonist naltrexone blocks acute endotoxic shock by inhibiting tumor necrosis factor-a production," Brain, Behavior, and Immunity, vol.
Li et al., "S-Amyrone inhibits lipopolysaccharide- induced inflammatory cytokines and protects against endotoxic shock in mice," Chemico-Biological Interactions, vol.
There is evidence supporting the immunoregulatory role of acyl-ghrelin [107] and its beneficial effects to treat chronic inflammatory syndromes, especially acyl-ghrelin immunoprotective properties during endotoxic shock [36].
(2006) Synthesis of lipid A monosaccharide analogues containing acidic amino acid: exploring the structural basis for the endotoxic and antagonistic activities.
Age-associated loss of immunomodulatory protection by granulocytecolony stimulating factor in endotoxic rats.
Moreover, animals under endotoxemia also develop an increase in glucocorticoid production that precedes that of insulin [27]; thus the enhanced glucocorticoid endogenous environment could be cooperating for maintaining glucose homeostasis [49], a phenomenon vital for survival during endotoxic shock.
We investigated: (i) the potential impact of Gram-negative bacterial STIs on the regulation of receptors involved in HIV infection in the cervix using the endotoxic component of the Gram-negative bacteria, lipopolysaccharide (LPS), as a mimetic of infection; and (ii) the potential molecular pathways underlying the action of LPS.
Endotoxic and anaphylactic-type shock in steers from intravenous injection of Escherichia coli endotoxin and ruminal absorption of endotoxin.
It may be worth mentioning here that presence of six and seven fatty acid acyl chains in heterogeneous distribution on bisphosphorylated ss-(1-6)-linked glucosamine disaccharide constitute highly endotoxic hexaacylated and heptaacylated lipid A species, which can excessively activate the host immune system to cause high fever, massive inflammation, septic shocks and ultimately death to the host [31].
It has been reported that the increased iNOS induced by ischemia/reperfusion injury or endotoxic shock in myocardium can be attenuated through PPAR-[delta] activation, the mechanism of which may implicate the influence of PPAR-[delta] on transcriptional control of iNOS expression [36, 37].