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dc.creatorMarch, Catalinaes_ES
dc.creatorMoranta, Davides_ES
dc.creatorRegueiro, Verónicaes_ES
dc.creatorLlobet, Enriquees_ES
dc.creatorTomás, Annaes_ES
dc.creatorGarmendia García, Juncales_ES
dc.creatorBengoechea Alonso, José Antonioes_ES
dc.date.accessioned2018-12-28T09:14:07Z
dc.date.available2018-12-28T09:14:07Z
dc.date.issued2011
dc.identifier.issn0021-9258 (Print)
dc.identifier.issn1083-351X (Electronic)
dc.identifier.urihttps://hdl.handle.net/2454/31893
dc.description.abstractOuter membrane protein A (OmpA) is a class of proteins highly conserved among the Enterobacteriaceae family and throughout evolution. Klebsiella pneumoniae is a capsulated Gram-negative pathogen. It is an important cause of community- acquired and nosocomial pneumonia. Evidence indicates that K. pneumoniae infections are characterized by a lack of an early inflammatory response. Data from our laboratory indicate that K. pneumoniae CPS helps to suppress the host inflammatory response. However, it is unknown whether K. pneumoniae employs additional factors to modulate host inflammatory responses. Here, we report that K. pneumoniaeOmpAis important for immune evasion in vitro and in vivo. Infection of A549 and normal human bronchial cells with 52OmpA2, an ompA mutant, increased the levels of IL-8. 52145- ΔwcaK2ompA, which does not express CPS and ompA, induced the highest levels of IL-8. Both mutants could be complemented. In vivo, 52OmpA2 induced higher levels of tnfα, kc, and il6 than the wild type. ompA mutants activated NF- κB, and the phosphorylation of p38, p44/42, and JNK MAPKs and IL-8 induction was via NF-κB-dependent and p38- and p44/42-dependent pathways. 52OmpA2 engaged TLR2 and -4 to activate NF-κB, whereas 52145- ΔwcaK2ompA activated not only TLR2 and TLR4 but also NOD1. Finally, we demonstrate that the ompA mutant is attenuated in the pneumonia mouse model. The results of this study indicate that K. pneumoniae OmpA contributes to attenuate airway cell responses. This may facilitate pathogen survival in the hostile environment of the lung.en
dc.description.sponsorshipThis work was supported by Fondo de Investigación Sanitaria Grant PI06/1629, ERA-NET Pathogenomics Grants GEN2006-27776-C2–2-E/PAT and SAF2008-04353-E, and Biomedicine Program Grant SAF2009-07885 from the Ministerio de Ciencia e Innovación (to J. A. B.).en
dc.format.extent12 p.
dc.format.mimetypeapplication/pdfen
dc.language.isoengen
dc.publisherAmerican Society for Biochemistry and Molecular Biologyen
dc.relation.ispartofJournal of Biological Chemistry, vol. 286, no. 12, pp. 9956–9967, March 25, 2011en
dc.rights© 2011 by The American Society for Biochemistry and Molecular Biology, Inc.en
dc.subjectKlebsiella pneumoniaeen
dc.subjectHost inflammatory responseen
dc.subjectAirway cell responsesen
dc.titleKlebsiella pneumoniae outer membrane protein A is required to prevent the activation of airway epithelial cellsen
dc.typeinfo:eu-repo/semantics/articleen
dc.typeArtículo / Artikuluaes
dc.contributor.departmentUniversidad Pública de Navarra. Instituto de Agrobiotecnologíaes_ES
dc.contributor.departmentNafarroako Unibertsitate Publikoa. Agrobioteknologiako Institutuaeu
dc.rights.accessRightsinfo:eu-repo/semantics/openAccessen
dc.rights.accessRightsAcceso abierto / Sarbide irekiaes
dc.identifier.doi10.1074/jbc.m110.181008
dc.relation.publisherversionhttps://doi.org/10.1074/jbc.m110.181008
dc.type.versioninfo:eu-repo/semantics/publishedVersionen
dc.type.versionVersión publicada / Argitaratu den bertsioaes


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