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MBC in Press, published online ahead of print May 29, 2003
Mol. Biol. Cell 10.1091/mbc.E02-12-0830

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Submitted on December 17, 2002
Accepted on April 25, 2003

Host but not parasite cholesterol controls Toxoplasma cell entry by modulating organelle discharge

Isabelle Coppens1* and Keith A. Joiner1

1 Department of Internal Medicine, Yale University School of Medicine, 808 LCI, 333 Cedar Street, P.O. Box 208022, New Haven, CT 06520-8022, USA

* Corresponding author. E-mail address: isabelle.coppens{at}yale.edu.

Host cell cholesterol is implicated in the entry and replication of an increasing number of intracellular microbial pathogens. While uptake of viral particles via cholesterol-enriched caveolae is increasingly well described, the requirement of cholesterol for internalization of eukaryotic pathogens is poorly understood and is likely to be partly organism-specific. We examined the role of cholesterol in active host cell invasion by the protozoan parasite Toxoplasma gondii. The parasitophorous vacuole membrane (PVM) surrounding T. gondii contains cholesterol at the time of invasion. Although cholesterol-enriched parasite apical organelles termed rhoptries discharge at the time of cell entry and contribute to PVM formation, surprisingly rhoptry cholesterol is not necessary for this process. In contrast, host plasma membrane cholesterol is incorporated into the forming PVM during invasion, through a caveolae-independent mechanism. Unexpectedly, depleting host cell plasma membrane cholesterol blocks parasite internalization by reducing the release of rhoptry proteins that are necessary for invasion. Cholesterol back-addition into host plasma membrane reverses this inhibitory effect of depletion on parasite secretion. These data define a new mechanism by which host cholesterol specifically controls entry of an intracellular pathogen.




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