Anti-Idiotype Monoclonal Antibodies as LPS Internal Images and Immunologic Protection Against Endotoxin Lethality in Mice
Gram negative bacterial infections continue to be a major cause of morbidity and mortality both in the United States and throughout the world (Anon). The existing evidence would strongly support the concept that, in many cases of Gram negative bacteremia and sepsis, endotoxic lipopolysaccharides (LPS) released from the microbial outer cell membrane are a major contributing factor to the pathophysiology of disease. In this respect, while LPS is generally regarded not to be directly toxic to host cells and tissues, it is potentially capable of stimulating cells to release a variety of inflammatory mediators, including tumor necrosis factor (TNF), many of the interleukins (Il-1, Il-6, Il-8, Il-10), products of phospholipid metabolism such as prostaglandins, leukotrienes and platelet activating factor (PAF) and procoagulant activity in the form of tissue factor (Morrison and Ryan, 1979). These biologically active mediators serve to promote a more generalized and often uncontrolled systemic inflammatory response which results in the hypotension, disseminated intra-vascular coagulation and multisystem organ failure characteristic of endotoxin shock.
KeywordsAffinity Column Coupling Buffer Eikenella Corrodens Immunologic Protection Mouse Myeloma Cell Line
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