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†The first two authors contributed equally to this study.
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The Salmonella pathogenicity island 1 secretion system directs cellular cholesterol redistribution during mammalian cell entry and intracellular trafficking
Article first published online: 20 MAR 2002
DOI: 10.1046/j.1462-5822.2002.00181.x
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How to Cite
Garner, M. J., Hayward, R. D. and Koronakis, V. (2002), The Salmonella pathogenicity island 1 secretion system directs cellular cholesterol redistribution during mammalian cell entry and intracellular trafficking. Cellular Microbiology, 4: 153–165. doi: 10.1046/j.1462-5822.2002.00181.x
Publication History
- Issue published online: 20 MAR 2002
- Article first published online: 20 MAR 2002
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Summary
The bacterial pathogen Salmonella triggers its own uptake into non-phagocytic mammalian cells. Entry is induced by the delivery of bacterial effector pro-teins 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 SPI2-encoded system.