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dc.creatorRochet, Elise 
dc.creatorArgy, Nicolas 
dc.creatorGreigert, Valentin 
dc.creatorBrunet, Julie 
dc.creatorSabou, Marcela 
dc.creatorMarcellin, Luc 
dc.creatorde-la-Torre, Alejandra 
dc.creatorSauer, Arnaud 
dc.creatorCandolfi, Ermanno 
dc.creatorPfaff, Alexander W. 
dc.date.accessioned2020-05-25T23:58:16Z
dc.date.available2020-05-25T23:58:16Z
dc.date.created2019
dc.identifier.issn19326203
dc.identifier.urihttps://repository.urosario.edu.co/handle/10336/22832
dc.description.abstractOcular toxoplasmosis (OT), mostly retinochorioditis, is a major feature of infection with the protozoan parasite Toxoplasma gondii. The pathophysiology of this infection is still largely elusive; especially mouse models are not yet well developed. In contrast, numerous in vitro studies showed the highly Toxoplasma strain dependent nature of the host-parasite interactions. Some distinct polymorphic virulence factors were characterized, notably the rhoptry protein ROP16. Here, we studied the strain-dependent pathophysiology in our OT mouse model. Besides of two wild type strains of the canonical I (RH, virulent) and II (PRU, avirulent) types, we used genetically engineered parasites, RH?ROP16 and PRU ROP16-I, expressing the type I allele of this virulence factor. We analyzed retinal integrity, parasite proliferation and retinal expression of cytokines. PRU parasites behaved much more virulently in the presence of a type I ROP16. In contrast, knockout of ROP16 in the RH strain led to a decrease of intraocular proliferation, but no difference in retinal pathology. Cytokine quantification in aqueous humor showed strong production of Th1 and inflammatory markers following infection with the two strains containing the ROP16-I allele. In strong contrast, immunofluorescence images showed that actual expression of most cytokines in retinal cells is rapidly suppressed by type I strain infection, with or without the involvement of its homologous ROP16 allele. This demonstrates the particular immune privileged situation of the retina, which is also revealed by the fact that parasite proliferation is nearly exclusively observed outside the retina. In summary, we further developed a promising OT mouse model and demonstrated the specific pathology in retinal tissues. © 2019 Rochet et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
dc.format.mimetypeapplication/pdf
dc.language.isoeng
dc.relation.ispartofPLoS ONE, ISSN:19326203, Vol.14, No.3 (2019)
dc.relation.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85063353108&doi=10.1371%2fjournal.pone.0214310&partnerID=40&md5=66ae4ca4de4bf27dcbb7667be6a8edce
dc.titleType I ROP16 regulates retinal inflammatory responses during ocular toxoplasmosis
dc.typearticle
dc.publisherPublic Library of Science
dc.subject.keywordCytokine
dc.subject.keywordanimal
dc.subject.keywordProtein rop16
dc.subject.keywordtoxoplasma gondii
dc.subject.keywordocular
dc.subject.keywordUnclassified drug
dc.subject.keywordVirulence factor
dc.subject.keywordCytokine
dc.subject.keywordProtein tyrosine kinase
dc.subject.keywordProtozoal protein
dc.subject.keywordRop16 protein
dc.subject.keywordAllele
dc.subject.keywordAnimal cell
dc.subject.keywordAnimal experiment
dc.subject.keywordAnimal model
dc.subject.keywordAqueous humor
dc.subject.keywordArticle
dc.subject.keywordCell proliferation
dc.subject.keywordChorioretinitis
dc.subject.keywordControlled study
dc.subject.keywordCytokine production
dc.subject.keywordFemale
dc.subject.keywordHistopathology
dc.subject.keywordImmunofluorescence
dc.subject.keywordMouse
dc.subject.keywordNonhuman
dc.subject.keywordOcular toxoplasmosis
dc.subject.keywordParasite virulence
dc.subject.keywordProtein expression
dc.subject.keywordRetina cell
dc.subject.keywordSequence homology
dc.subject.keywordTh1 cell
dc.subject.keywordTransgenic organism
dc.subject.keywordWild type
dc.subject.keywordAnimal
dc.subject.keywordClassification
dc.subject.keywordDisease model
dc.subject.keywordGenetic engineering
dc.subject.keywordGenetics
dc.subject.keywordImmunology
dc.subject.keywordMetabolism
dc.subject.keywordOcular toxoplasmosis
dc.subject.keywordParasitology
dc.subject.keywordPathogenicity
dc.subject.keywordRetina
dc.subject.keywordToxoplasma
dc.subject.keywordVirulence
dc.subject.keywordAnimals
dc.subject.keywordCytokines
dc.subject.keywordDisease models
dc.subject.keywordFemale
dc.subject.keywordGenetic engineering
dc.subject.keywordMice
dc.subject.keywordProtein-tyrosine kinases
dc.subject.keywordProtozoan proteins
dc.subject.keywordRetina
dc.subject.keywordToxoplasma
dc.subject.keywordToxoplasmosis
dc.subject.keywordVirulence
dc.rights.accesRightsinfo:eu-repo/semantics/openAccess
dc.type.spaArtículo
dc.rights.accesoAbierto (Texto Completo)
dc.type.hasVersioninfo:eu-repo/semantics/publishedVersion
dc.identifier.doihttps://doi.org/10.1371/journal.pone.0214310
dc.relation.citationIssueNo. 3
dc.relation.citationTitlePLoS ONE
dc.relation.citationVolumeVol. 14
dc.source.instnameinstname:Universidad del Rosario
dc.source.reponamereponame:Repositorio Institucional EdocUR


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