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2017-03-27Zeitschriftenartikel DOI: 10.1002/mbo3.469
Changes to cholesterol trafficking in macrophages by Leishmania parasites infection
dc.contributor.authorSemini, Geo
dc.contributor.authorPaape, Daniel
dc.contributor.authorPaterou, Athina
dc.contributor.authorSchroeder, Juliane
dc.contributor.authorBarrios-Llerena, Martin
dc.contributor.authorAebischer, Toni
dc.date.accessioned2018-05-07T19:56:22Z
dc.date.available2018-05-07T19:56:22Z
dc.date.created2017-04-07
dc.date.issued2017-03-27none
dc.identifier.otherhttp://edoc.rki.de/oa/articles/re87B89wloso/PDF/268l3mChcfIfU.pdf
dc.identifier.urihttp://edoc.rki.de/176904/2613
dc.description.abstractLeishmania spp. are protozoan parasites that are transmitted by sandfly vectors during blood sucking to vertebrate hosts and cause a spectrum of diseases called leishmaniases. It has been demonstrated that host cholesterol plays an important role during Leishmania infection. Nevertheless, little is known about the intracellular distribution of this lipid early after internalization of the parasite. Here, pulse-chase experiments with radiolabeled cholesteryl esterified to fatty acids bound to low-density lipoproteins indicated that retention of this source of cholesterol is increased in parasite-containing subcellular fractions, while uptake is unaffected. This is correlated with a reduction or absence of detectable NPC1 (Niemann–Pick disease, type C1), a protein responsible for cholesterol efflux from endocytic compartments, in the Leishmania mexicana habitat and infected cells. Filipin staining revealed a halo around parasites within parasitophorous vacuoles (PV) likely representing free cholesterol accumulation. Labeling of host cell membranous cholesterol by fluorescent cholesterol species before infection revealed that this pool is also trafficked to the PV but becomes incorporated into the parasites’ membranes and seems not to contribute to the halo detected by filipin. This cholesterol sequestration happened early after infection and was functionally significant as it correlated with the upregulation of mRNA-encoding proteins required for cholesterol biosynthesis. Thus, sequestration of cholesterol by Leishmania amastigotes early after infection provides a basis to understand perturbation of cholesterol-dependent processes in macrophages that were shown previously by others to be necessary for their proper function in innate and adaptive immune responses.eng
dc.language.isoeng
dc.publisherRobert Koch-Institut, Infektionskrankheiten / Erreger
dc.subject.ddc610 Medizin
dc.titleChanges to cholesterol trafficking in macrophages by Leishmania parasites infection
dc.typeperiodicalPart
dc.identifier.urnurn:nbn:de:0257-10052123
dc.identifier.doi10.1002/mbo3.469
dc.identifier.doihttp://dx.doi.org/10.25646/2538
local.edoc.container-titleMicrobiology Open
local.edoc.fp-subtypeArtikel
local.edoc.type-nameZeitschriftenartikel
local.edoc.container-typeperiodical
local.edoc.container-type-nameZeitschrift
local.edoc.container-urlhttp://onlinelibrary.wiley.com/doi/10.1002/mbo3.469/abstract
local.edoc.container-publisher-nameWiley
local.edoc.container-year2017

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