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dc.contributor.authorHyams, Catherine
dc.contributor.authorOpel, Sophia
dc.contributor.authorHanage, William
dc.contributor.authorYuste, Jose Enrique 
dc.contributor.authorBax, Katie
dc.contributor.authorHenriques-Normark, Birgitta
dc.contributor.authorSpratt, Brian G
dc.contributor.authorBrown, Jeremy S
dc.identifier.citationPLoS One. 2011;6(10):e24581.es_ES
dc.description.abstractBACKGROUND: Immunity to infections caused by Streptococcus pneumoniae is dependent on complement. There are wide variations in sensitivity to complement between S. pneumoniae strains that could affect their ability to cause invasive infections. Although capsular serotype is one important factor causing differences in complement resistance between strains, there is also considerable other genetic variation between S. pneumoniae strains that may affect complement-mediated immunity. We have therefore investigated whether genetically distinct S. pneumoniae strains with the same capsular serotype vary in their sensitivity to complement mediated immunity. METHODOLOGY AND PRINCIPAL FINDINGS: C3b/iC3b deposition and neutrophil association were measured using flow cytometry assays for S. pneumoniae strains with different genetic backgrounds for each of eight capsular serotypes. For some capsular serotypes there was marked variation in C3b/iC3b deposition between different strains that was independent of capsule thickness and correlated closely to susceptibility to neutrophil association. C3b/iC3b deposition results also correlated weakly with the degree of IgG binding to each strain. However, the binding of C1q (the first component of the classical pathway) correlated more closely with C3b/iC3b deposition, and large differences remained in complement sensitivity between strains with the same capsular serotype in sera in which IgG had been cleaved with IdeS. CONCLUSIONS: These data demonstrate that bacterial factors independent of the capsule and recognition by IgG have strong effects on the susceptibility of S. pneumoniae to complement, and could therefore potentially account for some of the differences in virulence between strains.es_ES
dc.description.sponsorshipThis work was undertaken at University College London, which received a proportion of funding from the Department of Health’s NIHR Biomedical Research Centre’s funding scheme. CH was supported by the Astor Foundation and Glaxo Smith Kline through the University College London MB PhD programme. JY was supported by the British Lung Foundation (P05/3). BHN is supported by the Ragnar and Torsten So¨ derberg foundation and the Swedish Research Council. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.es_ES
dc.publisherPublic Library of Sciencees_ES
dc.relation.isversionofPublisher's versiones_ES
dc.subject.meshAntibodies, Bacterial es_ES
dc.subject.meshBacterial Capsules es_ES
dc.subject.meshComplement C1q es_ES
dc.subject.meshComplement System Proteins es_ES
dc.subject.meshEnzyme-Linked Immunosorbent Assay es_ES
dc.subject.meshFlow Cytometry es_ES
dc.subject.meshHumans es_ES
dc.subject.meshImmunoglobulin G es_ES
dc.subject.meshNeutrophils es_ES
dc.subject.meshProtein Binding es_ES
dc.subject.meshSerotyping es_ES
dc.subject.meshStreptococcus pneumoniae es_ES
dc.titleEffects of Streptococcus pneumoniae strain background on complement resistancees_ES
dc.rights.licenseAtribución-NoComercial-CompartirIgual 4.0 Internacional*
dc.contributor.funderNational Institute for Health Research (United Kingdom)es_ES
dc.identifier.journalPloS onees_ES
dc.repisalud.centroISCIII::Centro Nacional de Microbiologíaes_ES

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