Interleukin-17-induced Protein Lipocalin 2 Is Dispensable For Immunity To Oral Candidiasis

dc.creatorFerreira M.C.
dc.creatorWhibley N.
dc.creatorMamo A.J.
dc.creatorSiebenlist U.
dc.creatorChan Y.R.
dc.creatorGaffen S.L.
dc.date2014
dc.date2015-06-25T17:50:12Z
dc.date2015-11-26T15:30:28Z
dc.date2015-06-25T17:50:12Z
dc.date2015-11-26T15:30:28Z
dc.date.accessioned2018-03-28T22:38:56Z
dc.date.available2018-03-28T22:38:56Z
dc.identifier
dc.identifierInfection And Immunity. , v. 82, n. 3, p. 1030 - 1035, 2014.
dc.identifier199567
dc.identifier10.1128/IAI.01389-13
dc.identifierhttp://www.scopus.com/inward/record.url?eid=2-s2.0-84894285479&partnerID=40&md5=a496a6439a375ec38b800b529388dd2b
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/85787
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/85787
dc.identifier2-s2.0-84894285479
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1261996
dc.descriptionOropharyngeal candidiasis (OPC; thrush) is an opportunistic fungal infection caused by the commensal microbe Candida albicans. Immunity to OPC is strongly dependent on CD4+ T cells, particularly those of the Th17 subset. Interleukin-17 (IL-17) deficiency in mice or humans leads to chronic mucocutaneous candidiasis, but the specific downstream mechanisms of IL-17- mediated host defense remain unclear. Lipocalin 2 (Lcn2; 24p3; neutrophil gelatinase-associated lipocalin [NGAL]) is an antimicrobial host defense factor produced in response to inflammatory cytokines, particularly IL-17. Lcn2 plays a key role in preventing iron acquisition by bacteria that use catecholate-type siderophores, and lipocalin 2-/- mice are highly susceptible to infection by Escherichia coli and Klebsiella pneumoniae. The role of Lcn2 in mediating immunity to fungi is poorly defined. Accordingly, in this study, we evaluated the role of Lcn2 in immunity to oral infection with C. albicans. Lcn2 is strongly upregulated following oral infection with C. albicans, and its expression is almost entirely abrogated in mice with defective IL-17 signaling (IL-17RA-/- or Act1-/- mice). However, Lcn2-/- mice were completely resistant to OPC, comparably to wild-type (WT) mice. Moreover, Lcn2 deficiency mediated protection from OPC induced by steroid immunosuppression. Therefore, despite its potent regulation during C. albicans infection, Lcn2 is not required for immunity to mucosal candidiasis. © 2014, American Society for Microbiology.
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dc.languageen
dc.publisher
dc.relationInfection and Immunity
dc.rightsaberto
dc.sourceScopus
dc.titleInterleukin-17-induced Protein Lipocalin 2 Is Dispensable For Immunity To Oral Candidiasis
dc.typeArtículos de revistas


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