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Capsule enlargement in Cryptococcus neoformans confers resistance to oxidative stress suggesting a mechanism for intracellular survival

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dc.contributor.authorZaragoza, Oscar
dc.contributor.authorChrisman, Cara J
dc.contributor.authorCastelli, Maria Victoria
dc.contributor.authorFrases, Susana
dc.contributor.authorCuenca-Estrella, Manuel
dc.contributor.authorRodriguez-Tudela, Juan Luis
dc.contributor.authorCasadevall, Arturo
dc.contributor.funderMinisterio de Educación y Ciencia (España)
dc.contributor.funderInstituto de Salud Carlos III
dc.date.accessioned2019-10-25T10:04:47Z
dc.date.available2019-10-25T10:04:47Z
dc.date.issued2008-10
dc.description.abstractCryptococcus neoformans is a facultative intracellular pathogen. The most distinctive feature of C. neoformans is a polysaccharide capsule that enlarges depending on environmental stimuli. The mechanism by which C. neoformans avoids killing during phagocytosis is unknown. We hypothesized that capsule growth conferred resistance to microbicidal molecules produced by the host during infection, particularly during phagocytosis. We observed that capsule enlargement conferred resistance to reactive oxygen species produced by H(2)O(2) that was not associated with a higher catalase activity, suggesting a new function for the capsule as a scavenger of reactive oxidative intermediates. Soluble capsular polysaccharide protected C. neoformans and Saccharomyces cerevisiae from killing by H(2)O(2). Acapsular mutants had higher susceptibility to free radicals. Capsular polysaccharide acted as an antioxidant in the nitroblue tetrazolium (NBT) reduction coupled to beta-nicotinamide adenine dinucleotide (NADH)/phenazine methosulfate (PMS) assay. Capsule enlargement conferred resistance to antimicrobial peptides and the antifungal drug Amphotericin B. Interestingly, the capsule had no effect on susceptibility to azoles and increased susceptibility to fluconazole. Capsule enlargement reduced phagocytosis by environmental predators, although we also noticed that in this system, starvation of C. neoformans cells produced resistance to phagocytosis. Our results suggest that capsular enlargement is a mechanism that enhances C. neoformans survival when ingested by phagocytic cells.es_ES
dc.description.peerreviewedSíes_ES
dc.description.sponsorshipWe thank Dr J.D. Nosanchuk for the use of defensins and Dr Steinman for the kind gift of A. castellanii strains. We thank Dr J.C. Arguelles and Pilar González (Universidad de Murcia, Spain) for providing protocols to measure catalase activity, and Drs Carlos and Juana Maria Gancedo (CSIC, Spain) for the permission to use their technical resources and for their helpful discussions. We are indebted to Dr F. Usera and Rosa Hidalgo for their collaboration, help and technical support in the use of the γ-irradiator from the animal facility from the National Center for Biotechnology (CSIC, Spain). We warmly thank Josefa Casas for her technical support, and all the members from the Mycology Service from the National Center for Microbiology (Instituto de Salud Carlos III) for their helpful discussions. M.V.C. is funded by a research contract from the Agencia Española de Cooperación Internacional (AECI). O.Z. is a ‘Ramón y Cajal’ fellow from the Ministerio Español de Educación y Ciencia (MEC) and is funded by Grants MPY1025/06 from the MEC and 1181/06 from el Instituto de Salud Carlos III.es_ES
dc.format.number10es_ES
dc.format.page2043-57es_ES
dc.format.volume10es_ES
dc.identifier.citationCell Microbiol. 2008 Oct;10(10):2043-57. doi: 10.1111/j.1462-5822.2008.01186.x. Epub 2008 Jun 28.es_ES
dc.identifier.doi10.1111/j.1462-5822.2008.01186.xes_ES
dc.identifier.e-issn1462-5822es_ES
dc.identifier.issn1462-5814es_ES
dc.identifier.journalCellular microbiologyes_ES
dc.identifier.pubmedID18554313es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/8530
dc.language.isoenges_ES
dc.publisherWileyes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/MPY1025/06es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/1181/06es_ES
dc.relation.publisherversionhttps://doi.org/10.1111/j.1462-5822.2008.01186.xes_ES
dc.repisalud.centroISCIII::Centro Nacional de Microbiologíaes_ES
dc.repisalud.institucionISCIIIes_ES
dc.rights.accessRightsopen accesses_ES
dc.rights.licenseAtribución-NoComercial-CompartirIgual 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.subject.meshAmphotericin Bes_ES
dc.subject.meshAnimalses_ES
dc.subject.meshAntifungal Agentses_ES
dc.subject.meshAntimicrobial Cationic Peptideses_ES
dc.subject.meshCatalasees_ES
dc.subject.meshColony Count, Microbiales_ES
dc.subject.meshCryptococcus neoformanses_ES
dc.subject.meshFungal Proteinses_ES
dc.subject.meshHydrogen Peroxidees_ES
dc.subject.meshMicrobial Viabilityes_ES
dc.subject.meshOxidantses_ES
dc.subject.meshPhagocytosises_ES
dc.subject.meshPolysaccharideses_ES
dc.subject.meshSaccharomyces cerevisiaees_ES
dc.subject.meshAdaptation, Physiologicales_ES
dc.subject.meshOxidative Stresses_ES
dc.titleCapsule enlargement in Cryptococcus neoformans confers resistance to oxidative stress suggesting a mechanism for intracellular survivales_ES
dc.typejournal articlees_ES
dc.type.hasVersionAMes_ES
dspace.entity.typePublication
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relation.isAuthorOfPublication459fc799-37e3-4fad-80fb-b134ccf72b7f
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relation.isAuthorOfPublication.latestForDiscovery298933e5-bfff-4e88-83ec-e4d2cb6581e1
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