Why is lps called an endotoxin

The first dye is blue or violet. It is followed by a decolorizing agent, and then the second dye, which is red. The bacteria that retains the color of the first dye are called gram positive.

The bacteria that lose the color of the first dye but retain the color of the second dye are called gram negative. LPS is also called an endotoxin because it is a toxin located inside the bacterial cell.

It was originally theorized that endotoxin is released once the bacteria dies. It is now a known fact that bacteria release small amounts of endotoxin as a part of their normal metabolism although the majority are still retained inside the cell.

The outermost structure is the O-antigen. It is called an antigen because it is the target for recognition for the host or human immune response. The O-antigen is a repetitive sequence of glycans. This sequence is variable and produces different kinds of O-antigens. There are known types in the bacteria E. Biologic differences such as these contribute to the overall variability in the testing of LAL.

The core domain simply contains multiple sugar chains as well as some non-carbohydrate components while the Lipid-A molecule is the least variable component of LPS. It anchors the LPS to the cell wall. Once the cell wall is degraded, Lipid-A is released from the bacterial cell and is the component responsible for the toxic effects of LPS on the human body.

Once inside the body, natural defense cells like macrophages and monocytes recognize the bacteria as foreign. This recognition process is mediated by the antigens in bacteria which include the O-antigen of LPS. The bacteria may sometimes evade destruction but are normally degraded by our defense cells. The endotoxins located within the bacteria are then released into the circulation and exert their deleterious effects. The defense cells of our body also release substances which may stimulate pathways that compound the negative effects of endotoxins.

The complement cascade, through substances C3a and C5a, causes the release of histamine, a major effector for the allergic response. The complement cascade generally causes vasodilation and inflammation. The inflammatory response is mediated through the release of substances which include the cytokines interleukins, prostaglandins and tumor necrosis factor. Interleukins are pyrogenic, they cause the febrile response. Naturally occurring subclinical endotoxemia in humans alters adaptive and innate immune functions through reduced MAPK and increased STAT1 phosphorylation.

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In vivo , Gram-negative bacteria probably release minute amounts of endotoxin while growing. This may be important in the stimulation of natural immunity.

It is known that small amounts of endotoxin may be released in a soluble form by young cultures grown in the laboratory. But for the most part, endotoxins remain associated with the cell wall until disintegration of the organisms. In vivo , this results from autolysis, external lysis mediated by complement and lysozyme, and phagocytic digestion of bacterial cells. Compared to the classic exotoxins of bacteria, endotoxins are less potent and less specific in their action, since they do not act enzymatically.

Endotoxins are heat stable boiling for 30 minutes does not destabilize endotoxin , but certain powerful oxidizing agents such as superoxide, peroxide and hypochlorite, have been reported to neutralize them. Endotoxins, although antigenic, cannot be converted to toxoids.

A comparison of the properties of bacterial endotoxins and classic exotoxins is shown in Table 1. Table 1. The function of the outer membrane of Gram-negative bacteria is to act as a protective permeability barrier.

The outer membrane is impermeable to large molecules and hydrophobic compounds from the environment. LPS is essential to the function of the outer membrane. First, it establishes a permeability barrier that is permeable only to low molecular weight, hydrophilic molecules.

In the E. This prevents penetration of the bacteria by bile salts and other toxic molecules from the GI tract. It also a barrier to lysozyme and many antimicrobial agents. Second, in an animal host, it may impede destruction of the bacterial cells by serum components and phagocytic cells. Third, LPS may play a role as an adhesin used in colonization of the host.

Lastly, variations in LPS structure provide for the existence of different antigenic strains of a pathogen that may be able to bypass a previous immunological response to a related strain. Most of the work on the chemical structure of endotoxin has been done with species of Salmonella and E. Lipopolysaccharides are complex amphiphilic molecules with a mw of about 10kDa, that vary widely in chemical composition both between and among bacterial species The general architecture of LPS is shown in Figure 2.

Region I. Lipid A is the lipid component of LPS. It contains the hydrophobic, membrane-anchoring region of LPS. Usually 6 FA are found. All FA in Lipid A are saturated. Some FA are attached directly to the NAG dimer and others are esterified to the 3-hydroxy fatty acids that are characteristically present. The structure of Lipid A is highly conserved among Gram-negative bacteria.

Among Enterobacteriaceae Lipid A is virtually constant. The primary structure of Lipid A has been elucidated and Lipid A has been chemically synthesized. Its biological activity appears to depend on a peculiar conformation that is determined by the glucosamine disaccharide, the PO 4 groups, the acyl chains, and also the KDO-containing inner core.