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dc.contributor.authorSánchez-Tarjuelo, Rodrigo 
dc.contributor.authorCortegano, Isabel 
dc.contributor.authorManosalva, Juliana 
dc.contributor.authorRodriguez-Garcia, Mercedes 
dc.contributor.authorRuiz, Carolina 
dc.contributor.authorAlía, Mario 
dc.contributor.authorPrado-Zamora, Maria Carmen 
dc.contributor.authorCano, Eva 
dc.contributor.authorFerrandiz-Avellano, Maria-Jose 
dc.contributor.authorde la Campa, Adela G 
dc.contributor.authorGaspar, Maria Luisa 
dc.contributor.authorAndres, Belen de 
dc.date.accessioned2020-10-06T09:02:00Z
dc.date.available2020-10-06T09:02:00Z
dc.date.issued2020-09-16
dc.identifier.citationFront. Immunol., 16 September 2020es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/11095
dc.description.abstractStreptococcus pneumoniae is the main cause of bacterial pneumonia, a condition that currently produces significant global morbidity and mortality. The initial immune response to this bacterium occurs when the innate system recognizes common motifs expressed by many pathogens, events driven by pattern recognition receptors like the Toll-like family receptors (TLRs). In this study, lung myeloid-cell populations responsible for the innate immune response (IIR) against S. pneumoniae, and their dependence on the TLR4-signaling axis, were analyzed in TLR4–/– and Myeloid-Differentiation factor-88 deficient (MyD88–/–) mice. Neutrophils and monocyte-derived cells were recruited in infected mice 3-days post-infection. Compared to wild-type mice, there was an increased bacterial load in both these deficient mouse strains and an altered IIR, although TLR4–/– mice were more susceptible to bacterial infection. These mice also developed fewer alveolar macrophages, weaker neutrophil infiltration, less Ly6Chigh monocyte differentiation and a disrupted classical and non-classical monocyte profile. The pro-inflammatory cytokine profile (CXCL1, TNF-α, IL-6, and IL-1β) was also severely affected by the lack of TLR4 and no induction of Th1 was observed in these mice. The respiratory burst (ROS production) after infection was profoundly dampened in TLR4–/– and MyD88–/– mice. These data demonstrate the complex dynamics of myeloid populations and a key role of the TLR4-signaling axis in the IIR to S. pneumoniae, which involves both the MyD88 and TRIF (Toll/IL-1R domain-containing adaptor-inducing IFN-β) dependent pathways.es_ES
dc.description.sponsorshipThis work was supported by grants of Ministerio de Ciencia SAF 2015-70880-R, RTI 2018-099114-B-100, BIO 2017-82951-R, and ISCIII PI14CIII/00049.es_ES
dc.language.isoenges_ES
dc.publisherFrontiers Media es_ES
dc.relation.isversionofPublisher's versiones_ES
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.titleThe TLR4-MyD88 Signaling Axis Regulates Lung Monocyte Differentiation Pathways in Response to Streptococcus pneumoniaees_ES
dc.typeArtículoes_ES
dc.rights.licenseAtribución 4.0 Internacional*
dc.identifier.pubmedID33042124
dc.format.volume11es_ES
dc.format.page2120es_ES
dc.identifier.doi10.3389/fimmu.2020.02120es_ES
dc.contributor.funderMinisterio de Ciencia e Innovación (España)
dc.contributor.funderInstituto de Salud Carlos III 
dc.description.peerreviewedes_ES
dc.identifier.e-issn1664-3224es_ES
dc.relation.publisherversionhttps://doi.org/10.3389/fimmu.2020.02120es_ES
dc.identifier.journalFrontiers in Immunologyes_ES
dc.repisalud.centroISCIII::Centro Nacional de Microbiologíaes_ES
dc.repisalud.centroISCIII::Instituto de Investigación de Enfermedades Rarases_ES
dc.repisalud.institucionISCIIIes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/SAF 2015-70880-Res_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/RTI 2018-099114-B-100es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/IO 2017-82951-Res_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/ISCIII PI14CIII/00049es_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES


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