细菌脂多糖发热是通过造血细胞上的Toll样受体4引发的。
Bacterial lipopolysaccharide fever is initiated via Toll-like receptor 4 on hematopoietic cells.
作者信息
Steiner Alexandre A, Chakravarty Sumana, Rudaya Alla Y, Herkenham Miles, Romanovsky Andrej A
机构信息
Systemic Inflammation Laboratory, Trauma Research, St Joseph's Hospital and Medical Center, 350 W Thomas Road, Phoenix, AZ 85013, USA.
出版信息
Blood. 2006 May 15;107(10):4000-2. doi: 10.1182/blood-2005-11-4743. Epub 2006 Jan 10.
Abstract
Lipopolysaccharide (LPS), a well-known bacterial pyrogen, is recognized by several receptors, including the Toll-like receptor 4 (TLR4), on various cells. Which of these receptors and cells are linked to fever production is unknown. By constructing 4 mouse chimeras and studying their thermoregulatory responses, we found that all 3 phases of the typical LPS fever depend on TLR4 signaling. The first phase is triggered via the TLR4 on hematopoietic cells. The second and third phases involve TLR4 signaling in both hematopoietic and nonhematopoietic cells.
摘要
脂多糖（LPS）是一种著名的细菌热原，可被多种细胞上的几种受体识别，包括Toll样受体4（TLR4）。这些受体和细胞中哪些与发热产生有关尚不清楚。通过构建4种小鼠嵌合体并研究它们的体温调节反应，我们发现典型LPS发热的所有3个阶段都依赖于TLR4信号传导。第一阶段是通过造血细胞上的TLR4触发的。第二和第三阶段涉及造血细胞和非造血细胞中的TLR4信号传导。
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