The Journal of Immunology · 2000 · 771 citations · 30 references
Life SciencesImmunologyInflammationInnate ImmunityMolecular ImmunologyCytokine BiologyInflammatory Response RegulationInflammatory SignalingInnate Immune Signaling PathwaysMacrophage BiologyToll-like ReceptorsEndotoxin ToleranceInflammatory Cytokine ProductionMacrophage Inflammatory ResponsesMyd88-dependent SignalingPeritoneal MacrophagesPretreatmentToll-like Receptor SignalingToll-like Receptor-mediated Innate Immune Response
Monocytes/macrophages exposed to LPS show reduced responses to second stimulation with LPS, which is termed LPS tolerance. In this study, we investigated molecular mechanism of LPS tolerance in macrophages. Mouse peritoneal macrophages pre-exposed to LPS exhibited reduced production of inflammatory cytokines in a time- and dose-dependent manner. Activation of neither IL-1 receptor-associated kinase nor NF-kappaB was observed in macrophages that became tolerant by LPS pretreatment, indicating that the proximal event in Toll-like receptor 4 (TLR4)-MyD88-dependent signaling is affected in tolerant macrophages. Although TLR4 mRNA expression significantly decreased within a few hours of LPS pretreatment and returned to the original level at 24 h, the surface TLR4 expression began to decrease within 1 h, with a gradual decrease after that, and remained suppressed over 24 h. A decrease in inflammatory cytokine production in tolerant macrophages well correlates with down-regulation of the surface TLR4 expression, which may explain one of the mechanisms for LPS tolerance.
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Defective LPS Signaling in C3H/HeJ and C57BL/10ScCr Mice: Mutations in <i>Tlr4</i> Gene
Alexander Poltorak, Xiaolong He, Irina Smirnova et al. · Science · 1998 · 7.6K citations
Katsuaki Hoshino, Osamu Takeuchi, Taro Kawai et al. · The Journal of Immunology · 1999 · 3.4K citations · Full text
Life Sciences, Genetics, Immunology +15