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Type I ROP16 regulates retinal inflammatory responses during ocular toxoplasmosis

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dc.creatorRochet, Elisespa
dc.creatorArgy, Nicolasspa
dc.creatorGreigert, Valentinspa
dc.creatorBrunet, Juliespa
dc.creatorSabou, Marcelaspa
dc.creatorMarcellin, Lucspa
dc.creatorde-la-Torre, Alejandraspa
dc.creatorSauer, Arnaudspa
dc.creatorCandolfi, Ermannospa
dc.creatorPfaff, Alexander W.spa
dc.date.accessioned2020-05-25T23:58:16Z
dc.date.available2020-05-25T23:58:16Z
dc.date.created2019spa
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.eng
dc.format.mimetypeapplication/pdf
dc.identifier.doihttps://doi.org/10.1371/journal.pone.0214310
dc.identifier.issn19326203
dc.identifier.urihttps://repository.urosario.edu.co/handle/10336/22832
dc.language.isoengspa
dc.publisherPublic Library of Sciencespa
dc.relation.citationIssueNo. 3
dc.relation.citationTitlePLoS ONE
dc.relation.citationVolumeVol. 14
dc.relation.ispartofPLoS ONE, ISSN:19326203, Vol.14, No.3 (2019)spa
dc.relation.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85063353108&doi=10.1371%2fjournal.pone.0214310&partnerID=40&md5=66ae4ca4de4bf27dcbb7667be6a8edcespa
dc.rights.accesRightsinfo:eu-repo/semantics/openAccess
dc.rights.accesoAbierto (Texto Completo)spa
dc.source.instnameinstname:Universidad del Rosariospa
dc.source.reponamereponame:Repositorio Institucional EdocURspa
dc.subject.keywordCytokinespa
dc.subject.keywordProtein rop16spa
dc.subject.keywordToxoplasma gondiieng
dc.subject.keywordOculareng
dc.subject.keywordUnclassified drugspa
dc.subject.keywordVirulence factorspa
dc.subject.keywordProtein tyrosine kinasespa
dc.subject.keywordProtozoal proteinspa
dc.subject.keywordRop16 proteineng
dc.subject.keywordAllelespa
dc.subject.keywordAnimal cellspa
dc.subject.keywordAnimal experimentspa
dc.subject.keywordAnimal modelspa
dc.subject.keywordAqueous humorspa
dc.subject.keywordCell proliferationspa
dc.subject.keywordChorioretinitisspa
dc.subject.keywordControlled studyspa
dc.subject.keywordCytokine productionspa
dc.subject.keywordFemalespa
dc.subject.keywordHistopathologyspa
dc.subject.keywordImmunofluorescencespa
dc.subject.keywordMousespa
dc.subject.keywordNonhumanspa
dc.subject.keywordOcular toxoplasmosisspa
dc.subject.keywordParasite virulencespa
dc.subject.keywordProtein expressionspa
dc.subject.keywordRetina cellspa
dc.subject.keywordSequence homologyspa
dc.subject.keywordTh1 cellspa
dc.subject.keywordTransgenic organismspa
dc.subject.keywordWild typespa
dc.subject.keywordClassificationspa
dc.subject.keywordDisease modelspa
dc.subject.keywordGenetic engineeringspa
dc.subject.keywordGeneticsspa
dc.subject.keywordImmunologyspa
dc.subject.keywordMetabolismspa
dc.subject.keywordOcular toxoplasmosisspa
dc.subject.keywordParasitologyspa
dc.subject.keywordPathogenicityspa
dc.subject.keywordRetinaspa
dc.subject.keywordToxoplasmaspa
dc.subject.keywordVirulencespa
dc.subject.keywordAnimalsspa
dc.subject.keywordCytokinesspa
dc.subject.keywordDisease modelseng
dc.subject.keywordFemalespa
dc.subject.keywordGenetic engineeringspa
dc.subject.keywordMicespa
dc.subject.keywordProtein-tyrosine kinasesspa
dc.subject.keywordProtozoan proteinsspa
dc.subject.keywordRetinaspa
dc.subject.keywordToxoplasmaspa
dc.subject.keywordToxoplasmosiseng
dc.subject.keywordVirulencespa
dc.titleType I ROP16 regulates retinal inflammatory responses during ocular toxoplasmosisspa
dc.typearticleeng
dc.type.hasVersioninfo:eu-repo/semantics/publishedVersion
dc.type.spaArtículospa
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