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dc.contributor.authorLópez López, José Ramón 
dc.contributor.authorAlpizar, Yeranddy A.
dc.contributor.authorMeseguer, Víctor
dc.contributor.authorEnoch, Luis
dc.contributor.authorTajada Esteban, Sendoa 
dc.contributor.authorDenlinger, Bristol
dc.contributor.authorFajardo, Otto
dc.contributor.authorManenschijn, Jan-Albert
dc.contributor.authorFernández Peña, Carlos
dc.contributor.authorTalavera, Arturo
dc.contributor.authorKichko, Tatiana
dc.contributor.authorNavia, Belén
dc.contributor.authorSánchez, Alicia
dc.contributor.authorSeñarís, Rosa
dc.contributor.authorReeh, Peter
dc.contributor.authorPérez García, María Teresa 
dc.contributor.authorVoets, Thomas
dc.contributor.authorBelmonte, Carlos
dc.contributor.authorTalavera, Karel
dc.contributor.authorViana, Felix
dc.date.accessioned2018-03-23T10:21:30Z
dc.date.available2018-03-23T10:21:30Z
dc.date.issued2014
dc.identifier.citationNature Communications, 2014, vol. 5. p. 1-16es
dc.identifier.issn2041-1723es
dc.identifier.urihttp://uvadoc.uva.es/handle/10324/29187
dc.descriptionProducción Científicaes
dc.description.abstractGram-negative bacterial infections are accompanied by inflammation and somatic or visceral pain. These symptoms are generally attributed to sensitization of nociceptors by inflammatory mediators released by immune cells. Nociceptor sensitization during inflammation occurs through activation of the Toll-like receptor 4 (TLR4) signalling pathway by lipopolysaccharide (LPS), a toxic by-product of bacterial lysis. Here we show that LPS exerts fast, membrane delimited, excitatory actions via TRPA1, a transient receptor potential cation channel that is critical for transducing environmental irritant stimuli into nociceptor activity. Moreover, we find that pain and acute vascular reactions, including neurogenic inflammation (CGRP release) caused by LPS are primarily dependent on TRPA1 channel activation in nociceptive sensory neurons, and develop independently of TLR4 activation. The identification of TRPA1 as a molecular determinant of direct LPS effects on nociceptors offers new insights into the pathogenesis of pain and neurovascular responses during bacterial infections and opens novel avenues for their treatment.es
dc.format.mimetypeapplication/pdfes
dc.language.isoenges
dc.publisherMacmillan Publisherses
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subject.classificationInfección bacterianaes
dc.subject.classificationPatogénesises
dc.titleTRPA1 channels mediate acute neurogenic inflammation and pain produced by bacterial endotoxinses
dc.typeinfo:eu-repo/semantics/articlees
dc.identifier.doi10.1038/ncomms4125es
dc.relation.publisherversionhttps://www.nature.com/articles/ncomms4125es
dc.identifier.publicationfirstpage1es
dc.identifier.publicationlastpage16es
dc.identifier.publicationtitleNature Communicationses
dc.identifier.publicationvolume5es
dc.peerreviewedSIes
dc.description.projectProjects SAF2010-14990 and PROMETEO2010-046. Instituto de Salud Carlos III. CONSOLIDER-INGENIO 2010. ISCIII grants R006/009 (Red Heracles), the Spanish Fundación Marcelino Botín and Belgian Federal Government (IUAP P6/28 and P7/13), the Research Foundation-Flanders and the Research Council of the KU Leuven.es
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 International


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