Endotoxin Signal Transduction Events and Mechanisms of Endotoxin Tolerance.
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概要
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Septic shock is caused by the systemic release of inflammatory mediators by various cell types but predominantly by macrophages and monocytes. The interaction of the gram negative bacterial products endotoxin (LPS) with macrophages causes the release of inflammatory mediators such as cytokines and arachidonic acid (AA) metabolites. These mediators, rather than LPS itself, are the major factor in the pathophysiology of septic shock. The intracellular transduction of signaling cascades activated by LPS, leading to production of cytokines and AA metabolites, remain to be clearly defined. However, several signaling molecules have been implicated, including tyrosine kinases, mitogen activated protein kinase (MAPK), GTP binding proteins, including Gαi and low molecular weight G (LMWG) proteins, protein kinase C (PKC), and transcription factors such as NFκB. One phenomenon that can have a profound effect on LPS, induced signal transduction is LPS tolerance. This condition is induced by pre-exposure of animals or LPS-responsive cells to low concentrations of LPS, which confers in vivo and in vitro cellular resistance to subsequent LPS stimulation. Signaling changes that occur in tolerant macrophages or monocytes include inhibited LPS, induced phosphorylation of the MAPK, extracellular regulated kinases (ERK) 1/2. The inhibition of phosphorylation appears to be a post-receptor event upstream of ERK. Since LPS tolerance induces resistance to LPS shock, as well as cross-tolerance to other noxious stimuli, on understanding of the molecular mechanisms of acquired tolerance may give rise to new therapeutic approaches to treat sepsis.
- 一般社団法人 日本救急医学会の論文
一般社団法人 日本救急医学会 | 論文
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