Lipopolysaccharide rapidly traffics to and from the golgi apparatus with the toll-like receptor 4-MD-2-CD14 complex in a process that is distinct from the initiation of signal transduction
Lipopolysaccharide rapidly traffics to and from the golgi apparatus with the toll-like receptor 4-MD-2-CD14 complex in a process that is distinct from the initiation of signal transduction
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DOI：
10.1074/jbc.m207873200
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发表时间：
2002-12-06
影响因子：
4.8
通讯作者：
Espevik, T
中科院分区：
文献类型：
--
作者：
Latz, E;Visintin, A;Espevik, T
哺乳动物对 LPS 的反应需要 Toll 样受体 4 (TLR4)、CD14 和 MD-2 的表达。我们在细胞系中表达荧光 TLR4，发现 TLR4 密集定位于表面和高尔基体。在人类单核细胞中观察到类似的分布。共焦成像显示高尔基体和质膜之间 TLR4-CD14-MD-2 复合物的快速循环。荧光 LPS 在 CD14 阳性细胞中遵循这些运输途径。 TLR4 适配器蛋白 MyD88 在 LPS 暴露以及表面 TLR4 与抗体诱导信号传导交联后易位至细胞表面。高尔基体相关的 TLR4 表达被布雷菲德菌素 A 破坏，但 LPS 信号传导得以保留。我们得出的结论是，LPS 信号传导可能是由 TLR4 的表面聚集启动的，并且不依赖于 LPS 向高尔基体的运输。
Mammalian responses to LPS require the expression of Toll-like receptor 4 (TLR4), CD14, and MD-2. We expressed fluorescent TLR4 in cell lines and found that TLR4 densely localized to the surface and the Golgi. Similar distributions were observed in human monocytes. Confocal imaging revealed rapid recycling of TLR4-CD14-MD-2 complexes between the Golgi and the plasma membrane. Fluorescent LPS followed these trafficking pathways in CD14-positive cells. The TLR4-adapter protein, MyD88, translocated to the cell surface upon LPS exposure, and cross-linking of surface TLR4 with antibody induced signaling. Golgi-associated TLR4 expression was disrupted by brefeldin A, yet LPS signaling was preserved. We conclude that LPS signaling may be initiated by surface aggregation of TLR4 and is not dependent upon LPS trafficking to the Golgi.