Protein A-mediated multicellular behavior in Staphylococcus aureus

dc.contributor.authorMerino Barberá, Nekane
dc.contributor.authorToledo Arana, Alejandro
dc.contributor.authorVergara Irigaray, Marta
dc.contributor.authorValle Turrillas, Jaione
dc.contributor.authorSolano Goñi, Cristina
dc.contributor.authorCalvo, Enrique
dc.contributor.authorLopez, Juan Antonio
dc.contributor.authorFoster, Timothy J.
dc.contributor.authorPenadés, José R.
dc.contributor.authorLasa Uzcudun, Íñigo
dc.contributor.departmentIdAB. Instituto de Agrobiotecnología / Agrobioteknologiako Institutuaes_ES
dc.date.accessioned2019-01-23T11:16:21Z
dc.date.available2019-01-23T11:16:21Z
dc.date.issued2008
dc.description.abstractThe capacity of Staphylococcus aureus to form biofilms on host tissues and implanted medical devices is one of the major virulence traits underlying persistent and chronic infections. The matrix in which S. aureus cells are encased in a biofilm often consists of the polysaccharide intercellular adhesin (PIA) or poly-N-acetyl glucosamine (PNAG). However, surface proteins capable of promoting biofilm development in the absence of PIA/PNAG exopolysaccharide have been described. Here, we used two-dimensional nano-liquid chromatography and mass spectrometry to investigate the composition of a proteinaceous biofilm matrix and identified protein A (spa) as an essential component of the biofilm; protein A induced bacterial aggregation in liquid medium and biofilm formation under standing and flow conditions. Exogenous addition of synthetic protein A or supernatants containing secreted protein A to growth media induced biofilm development, indicating that protein A can promote biofilm development without being covalently anchored to the cell wall. Protein A-mediated biofilm formation was completely inhibited in a dose-dependent manner by addition of serum, purified immunoglobulin G, or anti-protein A-specific antibodies. A murine model of subcutaneous catheter infection unveiled a significant role for protein A in the development of biofilm-associated infections, as the amount of protein A-deficient bacteria recovered from the catheter was significantly lower than that of wild-type bacteria when both strains were used to coinfect the implanted medical device. Our results suggest a novel role for protein A complementary to its known capacity to interact with multiple immunologically important eukaryotic receptors.en
dc.description.sponsorshipThis work was supported by the BIO2005-08399 and ERA-Net pathogenomics GEN2006-27792-C2-1-E/PAT grants from the Spanish Ministerio de Educación y Ciencia and grant LSHM-CT-2006-019064 from the European Union.en
dc.format.extent12 p.
dc.format.mimetypeapplication/pdfen
dc.identifier.doi10.1128/jb.01222-08
dc.identifier.issn0021-9193(Print)
dc.identifier.issn1098-5530 (Electronic)
dc.identifier.urihttps://academica-e.unavarra.es/handle/2454/32086
dc.language.isoengen
dc.publisherAmerican Society for Microbiologyen
dc.relation.ispartofJournal of Bacteriology, vol. 191, nº 3, feb. 2009, p. 832–843en
dc.relation.publisherversionhttps://doi.org/10.1128/jb.01222-08
dc.rights© 2009, American Society for Microbiology. All Rights Reserved.en
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess
dc.subjectStaphylococcus aureusen
dc.subjectStaphylococcal proteinen
dc.subjectMulticellular behavioren
dc.subjectBiofilmsen
dc.titleProtein A-mediated multicellular behavior in Staphylococcus aureusen
dc.typeinfo:eu-repo/semantics/article
dc.type.versioninfo:eu-repo/semantics/publishedVersion
dspace.entity.typePublication
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relation.isAuthorOfPublication.latestForDiscovery460895e1-d398-4878-9dc2-49ff15c440c7

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