Lipopolysaccharide endotoxicity

E. Th. Rietschel, L. Brade, B. Lindner and U. Zahringer. Bacterial Endotoxic Lipopolysaccharides. Vol. I. Molecular Biochemistry and Cellular Biology (D. C. Morrison, and J. L. Ryan, eds.) CRC Press, Boca Raton, Florida, p. 3-41 (1992). 

Snyderman, R., Gewurz, H., Mergenhagen, S.E. (1968). Interactions of the complement system with endotoxic lipopolysaccharide Generation of a factor chemotactic for polymorphonuclear leukocytes. J. Exp. Med 128,259-75. 

To set up and validate the in vitro systems we initiated a study with rat Uver slices. Stimulation by Upopolysaccharide (LPS) in liver slices was used to evoke a pro-inflammatory response in the Uver. Lipopolysaccharide (LPS), a component of Gram-negative bacterial ceU walls (also called endotoxin), has been associated with tissue injury and sepsis. In the Uver LPS activates the resident macrophages, the Kupffer ceUs, which results in cytokine release [96]. Furthermore, LPS is cleared by the Uver, mainly by Kupffer ceUs [97]. One of the major features of endotoxic shock is the induction of nitric oxide S5mthase in the Uver [98]. Inducible nitric oxide synthase (iNOS), the expression of which is induced by LPS and cytokines, produces nitric oxide (NO) in large quantities [99]. 

Lipid A. All R form lipopolysaccharides as well as free lipid A (obtained by mild acid cleavage of the KDO linkage) represent potent endotoxins, comparable in activity to complete lipopolysaccharides. This shows that lipid A represents the component of lipopolysaccharides which is responsible for its endotoxic properties. 

In animal models of acute renal failure induced in rats by bilateral nephrectomy and bilateral ureteral ligation, TAC increased, probably due to the accumulation of urate and uremic toxins with scavenging capacity, such as hyppurate (B19, S9). TAC of blood plasma was reduced in a rat endotoxic shock model (rats given i.p. 5 mg/kg lipopolysaccharide) (Cl6). 

Heine, H., Muller-Loennies, S., Brade, L., Lindner, B., Brade, H. Endotoxic activity and chemical structure of lipopolysaccharides from Chlamydia trachomatis serotypes E and L2 and Chlamydophila psittaci 6BC. Eur J Biochem 270 (2003) 440-450. 

Shnyra, A., Hultenby, K., Lindberg, A.A., Role of the physical state of Salmonella lipopolysaccharide in expression of biological and endotoxic properties. Infect Immun 61 (1993) 5351-5360. 

Moran, A.P., Schromm, A.B., Andra, J., Koch, M.H.J., Seydel, U., Brandenburg, K. Influence of endotoxic activity of Helicobacter pylori lipopolysaccharide on physicochemical parameters. Helicobacter 10 (2005b) 489. 

Rietschel, E.T., Brade, H., Brade, L., Brandenburg, K., Schade, U.F., Seydel, U., Z hringer U., Galanos, C., Ltideiitz, O., Westphal, O., Labischinski, H., Kusumoto, S., Shiba, T. Lipid A, the endotoxic center of bacterial lipopolysaccharides Relation of chemical structure to biological activity. Prog Clin Biol Res 231 (1987) 25-53. 

Takada, H., Kotuni, S. Structure function relationships of lipid, A. In Morrison, D.C., Ryan, J.L. (eds), Bacterial Endotoxic Lipopolysaccharides. CRC Press, Boca Raton, FL (1992), p. 107. 

Lipid A is the endotoxic principle of Gram-negative bacteria lipopolysaccharide. Its structure varies between bacteria. Sepsis could equally also be classed as immunomodulatory. 

Carbohydrates and their Derivatives, Including Tannins, Cellulose, and Related Lignins. Pergamon Elsevier, Oxford, 1999 Vol. 3, pp 179-239. Morrison DC and Ryan JL, eds. Bacterial Endotoxic Lipopolysaccharides,Vol 1 Molecular Biochemistry and Cellular Biology CRC Press, Boca Raton, EL, 1992 Vol. 1 449. 

Camenish TD, Koller BH. Earp HS, Matsushima GK. A novel receptor tyrosine kinase, Mer, inhibits TNFa production and lipopolysaccharide-induced endotoxic shock. J Immunol. 1999 162 3498-503. 

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