dc.contributor.author | Ramos-Sevillano, Elisa | |
dc.contributor.author | Rodriguez-Sosa, Cinthya | |
dc.contributor.author | Cafini, Fabio | |
dc.contributor.author | Giménez, Maria-Jose | |
dc.contributor.author | Navarro, Ana | |
dc.contributor.author | Sevillano, David | |
dc.contributor.author | Alou, Luis | |
dc.contributor.author | García, Ernesto | |
dc.contributor.author | Aguilar, Lorenzo | |
dc.contributor.author | Yuste, Jose Enrique | |
dc.date.accessioned | 2018-12-12T15:25:58Z | |
dc.date.available | 2018-12-12T15:25:58Z | |
dc.date.issued | 2012-09-05 | |
dc.identifier.citation | PLoS One. 2012;7(9):e44135 | es_ES |
dc.identifier.issn | 1932-6203 | es_ES |
dc.identifier.uri | http://hdl.handle.net/20.500.12105/6831 | |
dc.description.abstract | BACKGROUND: Specific antibodies mediate humoral and cellular protection against invading pathogens such as Streptococcus pneumoniae by activating complement mediated immunity, promoting phagocytosis and stimulating bacterial clearance. The emergence of pneumococcal strains with high levels of antibiotic resistance is of great concern worldwide and a serious threat for public health. METHODOLOGY/PRINCIPAL FINDINGS: Flow cytometry was used to determine whether complement-mediated immunity against three antibiotic-resistant S. pneumoniae clinical isolates is enhanced in the presence of sub-inhibitory concentrations of cefditoren and ceftriaxone. The binding of acute phase proteins such as C-reactive protein and serum amyloid P component, and of complement component C1q, to pneumococci was enhanced in the presence of serum plus either of these antibiotics. Both antibiotics therefore trigger the activation of the classical complement pathway against S. pneumoniae. C3b deposition was also increased in the presence of specific anti-pneumococcal antibodies and sub-inhibitory concentrations of cefditoren and ceftriaxone confirming that the presence of these antibiotics enhances complement-mediated immunity to S. pneumoniae. CONCLUSIONS/SIGNIFICANCE: Using cefditoren and ceftriaxone to promote the binding of acute phase proteins and C1q to pneumococci, and to increase C3b deposition, when anti-pneumococcal antibodies are present, might help reduce the impact of antibiotic resistance in S. pneumoniae infections. | es_ES |
dc.description.sponsorship | This work was supported by grants SAF2009-10824 from Dirección General de Investigación Científica y Técnica, MPY 1350/10 from ISCIII and an unrestricted educational grant from Tedec-Meiji Farma S. A. (Madrid, Spain). Centro de Investigación Biomédica en Red de Enfermedades Respiratorias (CIBERES) is an initiative of the ISCIII. E.R-S. was supported by an FPU fellowship from Ministerio de Ciencia e Innovación and C.R-S was supported by a fellowship from MAEC-AECID. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | Public Library of Science (PLOS) | es_ES |
dc.type.hasVersion | VoR | es_ES |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | * |
dc.subject.mesh | Acute-Phase Proteins | es_ES |
dc.subject.mesh | Animals | es_ES |
dc.subject.mesh | Anti-Bacterial Agents | es_ES |
dc.subject.mesh | Antibodies | es_ES |
dc.subject.mesh | Ceftriaxone | es_ES |
dc.subject.mesh | Cephalosporins | es_ES |
dc.subject.mesh | Complement Activation | es_ES |
dc.subject.mesh | Complement C1q | es_ES |
dc.subject.mesh | Complement C3c | es_ES |
dc.subject.mesh | Drug Resistance, Microbial | es_ES |
dc.subject.mesh | Egtazic Acid | es_ES |
dc.subject.mesh | Flow Cytometry | es_ES |
dc.subject.mesh | Humans | es_ES |
dc.subject.mesh | Immune System | es_ES |
dc.subject.mesh | Mice | es_ES |
dc.subject.mesh | Phagocytosis | es_ES |
dc.subject.mesh | Streptococcus pneumoniae | es_ES |
dc.subject.mesh | beta-Lactams | es_ES |
dc.title | Cefditoren and ceftriaxone enhance complement-mediated immunity in the presence of specific antibodies against antibiotic-resistant pneumococcal strains | es_ES |
dc.type | journal article | es_ES |
dc.rights.license | Atribución 4.0 Internacional | * |
dc.identifier.pubmedID | 22957048 | es_ES |
dc.format.volume | 7 | es_ES |
dc.format.number | 9 | es_ES |
dc.format.page | e44135 | es_ES |
dc.identifier.doi | 10.1371/journal.pone.0044135 | es_ES |
dc.contributor.funder | Ministerio de Ciencia e Innovación (España) | |
dc.contributor.funder | Instituto de Salud Carlos III | |
dc.contributor.funder | Tedec-Meiji Farma | |
dc.description.peerreviewed | Sí | es_ES |
dc.identifier.e-issn | 1932-6203 | es_ES |
dc.relation.publisherversion | https://doi.org/10.1371/journal.pone.0044135 | es_ES |
dc.identifier.journal | PloS one | es_ES |
dc.repisalud.centro | ISCIII::Centro Nacional de Microbiología | es_ES |
dc.repisalud.institucion | ISCIII | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/ES/SAF2009-10824 | es_ES |
dc.rights.accessRights | open access | es_ES |