The Salmonella pathogenicity island 1 secretion system directs cellular cholesterol redistribution during mammalian cell entry and intracellular trafficking
The Salmonella pathogenicity island 1 secretion system directs cellular cholesterol redistribution during mammalian cell entry and intracellular trafficking
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DOI：
10.1046/j.1462-5822.2002.00181.x
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发表时间：
2002-03-01
影响因子：
3.4
通讯作者：
Koronakis, V
中科院分区：
文献类型：
--
作者：
Garner, MJ;Hayward, RD;Koronakis, V
细菌病原体沙门氏菌触发其自身被非吞噬哺乳动物细胞吸收。尽管协调初始病原体-宿主细胞识别的分子机制仍知之甚少，但细菌效应蛋白的传递会破坏信号传导并促进细胞骨架重排，从而诱导进入。在这里，我们表明胆固醇对于沙门氏菌的吸收至关重要。质膜胆固醇的消耗和螯合特异性抑制细菌内化，但不抑制粘附。胆固醇在培养细胞的细菌进入位点积累，并在病原体内化后被含有沙门氏菌的液泡保留。细胞胆固醇重新分配需要由沙门氏菌致病岛 (SPI) 1 III 型分泌系统介导的细菌效应蛋白传递，但独立于 SP12 编码系统。
The bacterial pathogen Salmonella triggers its own uptake into non-phagocytic mammalian cells. Entry is induced by the delivery of bacterial effector proteins that subvert signalling and promote cytoskeletal rearrangement, although the molecular mechanisms that co-ordinate initial pathogen-host cell recognition remain poorly characterized. Here we show that cholesterol is essential for Salmonella uptake. Depletion and chelation of plasma membrane cholesterol specifically inhibited bacterial internalization but not adherence. Cholesterol accumulated at bacterial entry sites in cultured cells, and was retained by Salmonella-containing vacuoles following pathogen internalization. Cellular cholesterol redistribution required bacterial effector protein delivery mediated by the Salmonella pathogenicity island (SPI) 1 type III secretion system, but was independent of the SP12-encoded system.