The sepsis syndrome is thought to occur when microbial products activate Toll-like receptors stimulating widespread inflammation, in turn causing organ failure, shock and death. However, recent discoveries reveal that: (i) not only microbial substances but also endogenous molecules can trigger Toll-like receptors; (ii) Toll-like receptor-4, the endotoxin receptor, is constitutively suppressed; and (iii) the first step in sepsis could be the release of Toll-like receptor-4 from suppression. These discoveries suggest that endotoxin might not always initiate the sepsis syndrome and they explain why anti-endotoxin therapies fail. The discoveries also suggest new therapeutic targets - endogenous agonists and Toll-like receptor regulators - for treatment of sepsis.

译文

当微生物产物激活Toll样受体刺激广泛的炎症,进而导致器官衰竭,休克和死亡时,就会发生败血症综合征。然而,最近的发现表明 :( i) 不仅微生物物质,而且内源性分子都可以触发Toll样受体; (ii) Toll样受体-4 (内毒素受体) 被组成性抑制; (iii) 败血症的第一步可能是从抑制中释放Toll样受体4。这些发现表明内毒素可能并不总是引发败血症综合征,它们解释了抗内毒素疗法失败的原因。这些发现还提出了治疗脓毒症的新的治疗靶点-内源性激动剂和Toll样受体调节剂。

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