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Arch. Immunol. Ther. Exp. (Warsz.) · Feb 2012
ReviewMolecular mechanisms and pathological consequences of endotoxin tolerance and priming.
- Matthew Morris and Liwu Li.
- Department of Biological Sciences, Inflammation Biology and Immunobiology, Center for Inflammation, Virginia Tech, Blacksburg, VA 24061-0910, USA.
- Arch. Immunol. Ther. Exp. (Warsz.). 2012 Feb 1;60(1):13-8.
AbstractLipopolysaccharide (LPS), a component of Gram-negative bacteria, is a potent inflammatory stimulant, with high doses due to disseminated bacterial infection resulting in systemic inflammatory response syndrome and death. Lower doses can induce a state of tolerance to subsequent toxic doses of LPS, but extremely low doses have an opposite effect, priming the immune system for an even more violent response to subsequent challenge. A substantial body of research exists on the phenomenon of endotoxin tolerance, which appears to be a state of generalized dampening of inflammatory pathways. Comparatively little is known about the mechanisms or indeed the phenomenon of priming, particularly regarding the shift from a priming to a tolerizing response. Our aim is to review recent findings in the field of the inflammatory response to endotoxin, with a focus on highlighting the gaps in current understanding and attempting to reconcile the competing tolerance and priming phenomena.
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