Killing of Paracoccidioides brasiliensis yeast cells by IFN-gamma and TNF-alpha activated murine peritoneal macrophages: evidence of H(2)O(2) and NO effector mechanisms

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dc.contributor.authorMoreira, Ana Paula [UNESP]
dc.contributor.authorDias-Melicio, Luciane Alarcao [UNESP]
dc.contributor.authorPeraçoli, Maria Terezinha Serrão [UNESP]
dc.contributor.authorCalvi, Sueli Aparecida [UNESP]
dc.contributor.authorSoares, Ângela Maria Victoriano de Campos [UNESP]
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2014-05-20T13:34:30Z
dc.date.available2014-05-20T13:34:30Z
dc.date.issued2008-07-01
dc.description.abstractParacoccidioidomycosis is a deep mycosis, endemic in Latin America, caused by Paracoccidioides brasiliensis. Macrophage activation by cytokines is the major effector mechanism against this fungus. This work aimed at a better understanding of the interaction between yeast cells-murine peritoneal macrophages and the cytokine signals required for the effective killing of high virulence yeast-form of P. brasiliensis. In addition, the killing effector mechanisms dependent on the generation of reactive oxygen or nitrogen intermediates were investigated. Cell preincubation with IFN-gamma or TNF-alpha, at adequate doses, resulted in effective yeast killing as demonstrated in short-term (4-h) assays. Both, IFN-gamma and TNF-alpha activation were associated with higher levels of H(2)O(2) and NO when compared to nonactivation. Treatment with catalase (CAT), a H(2)O(2) scavenger, and N(G)-monomethyl-L-arginine (L-NMMA), a nitric oxide synthase inhibitor, reverted the killing effect of activated cells. Taken together, these results suggest that both oxygen and L-arginine-nitric oxide pathways play a role in the killing of highly virulent P. brasiliensis.en
dc.description.affiliationUniv Estadual Paulista, Dept Microbiol & Immunol, Biosci Inst, BR-18618000 São Paulo, Brazil
dc.description.affiliationUniv Estadual Paulista, Dept Trop Dis & Image Diag, Botucatu Med Sch, BR-18618000 São Paulo, Brazil
dc.description.affiliationUnespUniv Estadual Paulista, Dept Microbiol & Immunol, Biosci Inst, BR-18618000 São Paulo, Brazil
dc.description.affiliationUnespUniv Estadual Paulista, Dept Trop Dis & Image Diag, Botucatu Med Sch, BR-18618000 São Paulo, Brazil
dc.format.extent17-23
dc.identifierhttp://dx.doi.org/10.1007/s11046-007-9046-3
dc.identifier.citationMycopathologia. Dordrecht: Springer, v. 166, n. 1, p. 17-23, 2008.
dc.identifier.doi10.1007/s11046-007-9046-3
dc.identifier.issn0301-486X
dc.identifier.lattes2179450022699059
dc.identifier.lattes6486557387397806
dc.identifier.urihttp://hdl.handle.net/11449/11838
dc.identifier.wosWOS:000257215400002
dc.language.isoeng
dc.publisherSpringer
dc.relation.ispartofMycopathologia
dc.relation.ispartofjcr1.476
dc.rights.accessRightsAcesso restrito
dc.sourceWeb of Science
dc.subjectParacoccidioidomycosisen
dc.subjectmurine macrophagesen
dc.subjectfungicidal activityen
dc.subjectcytokinesen
dc.subjectNOen
dc.subjectH(2)O(2)en
dc.titleKilling of Paracoccidioides brasiliensis yeast cells by IFN-gamma and TNF-alpha activated murine peritoneal macrophages: evidence of H(2)O(2) and NO effector mechanismsen
dc.typeArtigo
dcterms.licensehttp://www.springer.com/open+access/authors+rights?SGWID=0-176704-12-683201-0
dcterms.rightsHolderSpringer
unesp.author.lattes2179450022699059
unesp.author.lattes6486557387397806
unesp.author.orcid0000-0002-0936-9512[3]
unesp.author.orcid0000-0001-9254-2074[2]
unesp.author.orcid0000-0003-1962-9901[5]
unesp.campusUniversidade Estadual Paulista (Unesp), Faculdade de Medicina, Botucatupt

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