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dc.creatorEuba, Begoñaes_ES
dc.creatorMoleres Apilluelo, Javieres_ES
dc.creatorViadas Martínez, Cristinaes_ES
dc.creatorRuiz de los Mozos Aliaga, Igores_ES
dc.creatorValle Turrillas, Jaionees_ES
dc.creatorBengoechea Alonso, José Antonioes_ES
dc.creatorGarmendia García, Juncales_ES
dc.date.accessioned2018-09-06T12:20:22Z
dc.date.available2018-09-06T12:20:22Z
dc.date.issued2015
dc.identifier.issn1932-6203
dc.identifier.urihttps://hdl.handle.net/2454/30554
dc.description.abstractNontypable Haemophilus influenzae (NTHi) is a major cause of opportunistic respiratory tract disease, and initiates infection by colonizing the nasopharynx. Bacterial surface proteins play determining roles in the NTHi-airways interplay, but their specific and relative contribution to colonization and infection of the respiratory tract has not been addressed comprehensively. In this study, we focused on the ompP5 and hap genes, present in all H. influenzae genome sequenced isolates, and encoding the P5 and Hap surface proteins, respectively. We employed isogenic single and double mutants of the ompP5 and hap genes generated in the pathogenic strain NTHi375 to evaluate P5 and Hap contribution to biofilm growth under continuous flow, to NTHi adhesion, and invasion/phagocytosis on nasal, pharyngeal, bronchial, alveolar cultured epithelial cells and alveolar macrophages, and to NTHi murine pulmonary infection.We show that P5 is not required for bacterial biofilm growth, but it is involved in NTHi interplay with respiratory cells and in mouse lung infection. Mechanistically, P5NTHi375 is not a ligand for CEACAM1 or α5 integrin receptors. Hap involvement in NTHi375-host interaction was shown to be limited, despite promoting bacterial cell adhesion when expressed in H. influenzae RdKW20.We also show that Hap does not contribute to bacterial biofilm growth, and that its absence partially restores the deficiency in lung infection observed for the ΔompP5 mutant. Altogether, this work frames the relative importance of the P5 and Hap surface proteins in NTHi virulence.en
dc.description.sponsorshipThis study was supported by ISCIII PS09/00130, Ministerio Economía y Competitividad-MINECO SAF2012-31166, Dpto. Salud Gobierno Navarra 359/2012, CIBERES.en
dc.format.mimetypeapplication/pdfen
dc.format.mimetypeapplication/zipen
dc.language.isoengen
dc.publisherPublic Library of Scienceen
dc.relation.ispartofPlos One, 10(4): e0123154en
dc.rights© 2015 Euba et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.en
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subjectNontypable Haemophilus influenzae (NTHi)en
dc.subjectompP5 genesen
dc.subjectHap genesen
dc.titleRelative contribution of P5 and hap surface proteins to nontypable haemophilus influenzae interplay with the host upper and lower airwaysen
dc.typeinfo:eu-repo/semantics/articleen
dc.typeArtículo / Artikuluaes
dc.contributor.departmentIdAB – Instituto de Agrobiotecnología / Agrobioteknologiako Institutuaes
dc.rights.accessRightsinfo:eu-repo/semantics/openAccessen
dc.rights.accessRightsAcceso abierto / Sarbide irekiaes
dc.identifier.doi10.1371/journal.pone.0123154
dc.identifier.doi10.1371/journal.pone.0123154.s001
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/6PN/SAF2012-31166en
dc.relation.publisherversionhttps://doi.org/10.1371/journal.pone.0123154
dc.type.versioninfo:eu-repo/semantics/publishedVersionen
dc.type.versionVersión publicada / Argitaratu den bertsioaes
dc.contributor.funderGobierno de Navarra / Nafarroako Gobernua, 359/2012es


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© 2015 Euba et al. This is an open
access article distributed under the terms of the
Creative Commons Attribution License, which permits
unrestricted use, distribution, and reproduction in any
medium, provided the original author and source are
credited.
Except where otherwise noted, this item's license is described as © 2015 Euba et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.