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Gram-negative endotoxin

Anti-Gram-negative endotoxin Products
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- Type: Mouse antibody
- Application: ELISA
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- Type: Mouse antibody
- Application: ELISA
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- Type: Mouse antibody
- Application: Indirect ELISA
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- Type: Mouse antibody
- Application: ELISA
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- Type: Mouse antibody
- Application: ELISA
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- Type: Mouse antibody
- Application: ELISA
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- Type: Mouse antibody
- Application: Indirect ELISA
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- Type: Mouse antibody
- Application: ELISA
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- Type: Mouse antibody
- Application: ELISA
- Mouse Anti-Gram-negative Endotoxin Antibody, mRNA (MRO-286-MZ-mRNA) (MRO-286-MZ-mRNA)
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- Species Reactivity: Gram-negative bacteria
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For Research Use Only. Not For Clinical Use.
Endotoxins, also known as lipopolysaccharides (LPS), are large molecules consisting of O antigen (or O polysaccharide), core oligosaccharide, and lipid A. They are found in the outer membrane of Gram-negative bacteria. LPS is the major component of the outer membrane of Gram-negative bacteria, contributing greatly to the structural integrity of the bacteria, and protecting the membrane from certain kinds of chemical attack. LPS also increases the negative charge of the cell membrane and helps stabilize the overall membrane structure. It is of crucial importance to many Gram-negative bacteria, which die if it is mutated or removed. However, it appears that LPS is nonessential in at least some Gram-negative bacteria, such as Neisseria meningitidis, Moraxella catarrhalis, and Acinetobacter baumannii. LPS induces a strong response from normal animal immune systems. It has also been implicated in non-pathogenic aspects of bacterial ecology, including surface adhesion, bacteriophage sensitivity, and interactions with predators such as amoebae. The presence of endotoxins in the blood is called endotoxemia. It can lead to septic shock, if the immune response is severely pronounced. Lipid A may cause uncontrolled activation of mammalian immune systems with production of inflammatory mediators that may lead to septic shock. The molecular mimicry of some LOS molecules is thought to cause autoimmune-based host responses, such as flareups of multiple sclerosis. Epidemiological studies have previously shown that increased endotoxin load, which can be a result of increased populations of endotoxin producing bacteria in the intestinal tract, is associated with certain obesity-related patient groups.
