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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 ?
Microbial agents such as endotoxin [or lipopolysaccharide (LPS)], part of the outer membrane of Gram-negative bacteria (Bos and Tommassen 2004), and (1 [right arrow] 3)-[beta]-D-glucan, a fungal cell wall constituent, have been associated with adverse respiratory health outcomes (Adhikari et al.
Friedrich will be presenting a spotlight session on "Low Endotoxin Recovery" (LER) on day one.
Biochemical principle of Limulus test for detecting bacterial endotoxins. Proc Jpn Acad Ser B Phys Biol Sci 83, 110-119.
The FDA issued guidance on endotoxins in June 2012.
Endotoxins are heat-stable and, therefore, usual sterilization processes are ineffective for their destruction.
As is known to us, LPS could activate the PI3K/AKT pathway, which regulates the expressions of cytokine and chemokine, such as TNF-[alpha] [8-10], moreover, which is involved in endotoxin tolerance [11].
It is normal for small amounts of endotoxins to cross the intestinal barrier into the circulation; they are regulated and removed by reticuloendothelial cells, phagocytes in the liver [38], mesenteric lymph nodes [39], anti-endotoxin antibodies [38,40,41], and lipoproteins [42].
Objective: To examine the effects of airborne endotoxin on lung function impairment in exposure-response relationships among the workers of textile industry.
The aim of this study was to assess exposure to airborne endotoxins and peptidoglycans as well as to assess the possibility to use PGs as a surrogate measure of bacterial exposure in workplaces in a metal processing plant in comparison with another inflammatory marker, i.e., endotoxins.
In vitro experiments have shown that endotoxins are transported from the gastrointestinal tract into the peripheral circulation, in particular through the ruminal wall at a greater speed than in the colon wall but at pH acids, increasing 5 to 6 times permeability through the colon and ruminal tissues and allowing the passage of large molecules (16).
Cautions were taken to minimize the interference by non PM-originated endotoxins. Before a sampling trip, Harvard impactors and other sampling devices (e.g., filter cassettes and tubing) were cleaned with 70% isopropanol and then dried under a UV light in a biosafety cabinet; Teflon membrane filters were exposed to UV light for at least 60 min.