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dc.contributor.authorMeseguer, Victor
dc.contributor.authorAlpizar, Yeranddy A.
dc.contributor.authorLuis, Enoch
dc.contributor.authorTajada, 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.authorLópez-López, José Ramón
dc.contributor.authorVoets, Thomas
dc.contributor.authorBelmonte, Carlos
dc.contributor.authorTalavera, Karel
dc.contributor.authorViana, Félix
dc.date.accessioned2024-02-06T09:39:31Z
dc.date.available2024-02-06T09:39:31Z
dc.date.issued2014
dc.identifier.citationNat Commun. 2014;5:3125.es
dc.identifier.urihttps://uvadoc.uva.es/handle/10324/65782
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.isospaes
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses
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.identifier.publicationissue1es
dc.identifier.publicationtitleNature Communicationses
dc.identifier.publicationvolume5es
dc.peerreviewedSIes
dc.identifier.essn2041-1723es
dc.type.hasVersioninfo:eu-repo/semantics/draftes


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