Sequestration and Tissue Accumulation of Human Malaria Parasites Can We Learn Anything from Rodent Models of Malaria 英文参考文献.docVIP

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Sequestration and Tissue Accumulation of Human Malaria Parasites Can We Learn Anything from Rodent Models of Malaria 英文参考文献.doc

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Sequestration and Tissue Accumulation of Human Malaria Parasites Can We Learn Anything from Rodent Models of Malaria 英文参考文献

Review SequestrationandTissueAccumulationofHuman MalariaParasites:CanWeLearnAnythingfromRodent ModelsofMalaria? BlandineFranke-Fayard,JannikFonager,AnnekeBraks,ShahidM.Khan,ChrisJ.Janse* LeidenMalariaResearchGroup,DepartmentofParasitology,CenterofInfectiousDiseases,LeidenUniversityMedicalCenter,Leiden,TheNetherlands statesinrodentssuchascerebralcomplicationsinseveralstrainsof mice[18–23],pregnancy-associatedpathology[24–26],andacute Abstract: The sequestration of Plasmodium falciparum– infectedredbloodcells(irbcs)inthemicrovasculatureof organsisassociatedwithseveredisease;correspondingly, themolecularbasisofirbcadherenceisanactiveareaof study. In contrast to P. falciparum, much less is known about sequestration in other Plasmodium parasites, lung injury [27,28]. To what extent these different pathologies observed in laboratory animals are representative for human pathology is a matter of debate and has been discussed in a number of review papers [8,9,19,21,25,26,29–33]. Based on a number of differences in clinical features of human cerebral includingthosespeciesthatareusedasmodelstostudy malaria(HCM)causedbyP.falciparumandthecerebralpathology severe malaria. Here, we review the cytoadherence of P. berghei infections in mice, the relevance of P. berghei for properties of irbcs of the rodent parasite Plasmodium understandingHCMhasbeenbroughtintoquestion.However,it berghei ANKA, where schizonts demonstrate a clear isevidentthatstudiesonso-calledexperimentalcerebralmalaria (ECM)inducedbyP.bergheihaveprovidedinsightsintothecritical rolethatavarietyofhostimmunefactorsplayininducingcerebral sequestration phenotype. Real-time in vivo imaging of transgenic P. berghei parasites in rodents has revealed a CD36-dependent sequestration in lungs and adipose pathology in mice. It has been argued that this knowledge may indeed be relevant for understanding, at least in part, the pathologyassociatedwithHCM,asthehumanconditionitselfis likely to represent a spectrum of pathol