title: Molecular mechanisms of innate memory and tolerance to LPS.
abstract: LPS is a potent trigger of macrophage-mediated inflammation. However, prolonged exposure to LPS induces a state of tolerance that reprograms the inflammatory response, resulting in reduced inflammatory cytokine production in vitro and in vivo. Recent evidence suggests that LPS tolerance also increases the expression of a subset of genes that may protect animals from systemic infection while they are in the tolerized state. However, a molecular basis for these selective changes in inflammatory gene expression during LPS tolerance has remained elusive. In this review, we discuss the molecular mechanisms that may account for these effects, focusing on changes in LPS signaling, epigenetic markers, and chromatin remodeling that may be responsible for cellular memory and physiologic changes that comprise the LPS tolerance phenomenon.
authors: Department of Microbiology and Immunology, Columbia University, College of Physicians and Surgeons, New York, New York, USA.
authors: John J
authors: JJ
authors: Seeley
authors: Department of Microbiology and Immunology, Columbia University, College of Physicians and Surgeons, New York, New York, USA sg2715@columbia.edu.
authors: Sankar
authors: S
authors: Ghosh
mesh_terms: D000818:Animals; D019175:DNA Methylation / Q000235:genetics; D006801:Humans; D007108:Immune Tolerance / Q000276:immunology*; D007113:Immunity, Innate; D007156:Immunologic Memory; D008070:Lipopolysaccharides / Q000276:immunology*; D051193:Toll-Like Receptors / Q000378:metabolism
chemical_list: D008070:Lipopolysaccharides; D051193:Toll-Like Receptors
keywords: chromatin; endotoxin; epigenetics; inflammation; lipopolysaccharide