Host cell traversal is important for progression of the malaria parasite through the dermis to the liver

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dc.contributor.authorAmino, Rogerio [UNIFESP]
dc.contributor.authorGiovannini, Donatella
dc.contributor.authorThiberge, Sabine
dc.contributor.authorGueirard, Pascale
dc.contributor.authorBoisson, Bertrand
dc.contributor.authorDubremetz, Jean-Francois
dc.contributor.authorPrevost, Marie-Christine
dc.contributor.authorIshino, Tomoko
dc.contributor.authorYuda, Masao
dc.contributor.authorMenard, Robert
dc.contributor.institutionInst Pasteur
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionUniv Montpellier 2
dc.contributor.institutionMie Univ
dc.date.accessioned2016-01-24T13:49:29Z
dc.date.available2016-01-24T13:49:29Z
dc.date.issued2008-02-01
dc.description.abstractThe malaria sporozoite, the parasite stage transmitted by the mosquito, is delivered into the dermis and differentiates in the liver. Motile sporozoites can invade host cells by disrupting their plasma membrane and migrating through them (termed cell traversal), or by forming a parasite-cell junction and settling inside an intracellular vacuole (termed cell infection). Traversal of liver cells, observed for sporozoites in vivo, is thought to activate the sporozoite for infection of a final hepatocyte. Here, using Plasmodium berghei, we show that cell traversal is important in the host dermis for preventing sporozoite destruction by phagocytes and arrest by nonphagocytic cells. We also show that cell infection is a pathway that is masked, rather than activated, by cell traversal. We propose that the cell traversal activity of the sporozoite must be turned on for progression to the liver parenchyma, where it must be switched off for infection of a final hepatocyte.en
dc.description.affiliationInst Pasteur, Unite Biol & Genet Paludisme, F-75724 Paris 15, France
dc.description.affiliationUniversidade Federal de São Paulo, Dept Bioquim, BR-04044020 São Paulo, Brazil
dc.description.affiliationUniv Montpellier 2, CNRS, UMR 5539, F-34095 Montpellier 05, France
dc.description.affiliationMie Univ, Sch Med, Tsu, Mie 5140001, Japan
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Bioquim, BR-04044020 São Paulo, Brazil
dc.description.sourceWeb of Science
dc.format.extent88-96
dc.identifierhttp://dx.doi.org/10.1016/j.chom.2007.12.007
dc.identifier.citationCell Host & Microbe. Cambridge: Cell Press, v. 3, n. 2, p. 88-96, 2008.
dc.identifier.doi10.1016/j.chom.2007.12.007
dc.identifier.fileWOS000253302100006.pdf
dc.identifier.issn1931-3128
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/30386
dc.identifier.wosWOS:000253302100006
dc.language.isoeng
dc.publisherCell Press
dc.relation.ispartofCell Host & Microbe
dc.rightsinfo:eu-repo/semantics/openAccess
dc.titleHost cell traversal is important for progression of the malaria parasite through the dermis to the liveren
dc.typeinfo:eu-repo/semantics/article
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