title: Molecular mechanisms and pathological consequences of endotoxin tolerance and priming.
abstract: Lipopolysaccharide (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.
authors.affiliation: Department of Biological Sciences, Inflammation Biology and Immunobiology, Center for Inflammation, Virginia Tech, Blacksburg, VA 24061-0910, USA.
authors.forename: Matthew
authors.initials: M
authors.lastname: Morris
authors.forename: Liwu
authors.initials: L
authors.lastname: Li
mesh_terms: D000818:Animals; D004731:Endotoxins / Q000276:immunology* / Q000494:pharmacology; D006801:Humans; D007108:Immune Tolerance / Q000187:drug effects / Q000276:immunology*; D007249:Inflammation / Q000276:immunology; D008070:Lipopolysaccharides / Q000276:immunology* / Q000494:pharmacology; D015398:Signal Transduction / Q000276:immunology; D018746:Systemic Inflammatory Response Syndrome / Q000276:immunology
chemical_list: D004731:Endotoxins; D008070:Lipopolysaccharides