脂多糖的病理生物学。

P R Mayeux
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引用次数: 210

摘要

脂多糖是革兰氏阴性细菌细胞壁的一种成分,在美国每年造成25000 - 50000人死亡。革兰氏阴性感染和败血症导致死亡的后遗症包括发热、低血压、组织灌注不足和弥散性血管内凝血。很明显,不同的细胞类型对脂多糖的反应不同。此外,各种类脂素和细胞因子被释放,甚至在不识别脂多糖的细胞类型中也能影响细胞功能。尽管在感染性休克和器官衰竭的病因学方面取得了进展,但治疗在很大程度上仍然是支持性的,而且很大程度上是无效的。本综述的目的是通过检查信号转导和治疗方法来总结目前对脂多糖在败血症发展中的作用的理解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Pathobiology of lipopolysaccharide.

Lipopolysaccharide is a component of the gram-negative bacterial cell wall that is responsible for 25,000-50,000 deaths in the United States each year. The sequelae of gram-negative infection and septicemia leading to death include fever, hypotension with inadequate tissue perfusion, and disseminated intravascular coagulation. It is clear that different cell types respond differently to lipopolysaccharide. Furthermore, various autacoids and cytokines are released that can affect cellular function even in cell types that do not recognize lipopolysaccharide. Despite advances made in the etiology of septic shock and organ failure, therapy is still for the most part supportive and largely ineffective. The aim of this review is to summarize the current understanding of the role of lipopolysaccharide in the development of septicemia by examining signal transduction and therapeutic approaches.

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