Neutrophils engage the kallikrein-kinin system to open up the endothelial barrier in acute inflammation

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dc.contributorLaboratório de Desenvolvimento de Vacinaspt_BR
dc.contributorCentro de Biotecnologiapt_BR
dc.contributor.authorKenne, Ellinorpt_BR
dc.contributor.authorRasmuson, Joelpt_BR
dc.contributor.authorRenné, Thomaspt_BR
dc.contributor.authorVieira, Mônica Laruccipt_BR
dc.contributor.authorMüller-Esterl, Wernerpt_BR
dc.contributor.authorHerwald, Heikopt_BR
dc.contributor.authorLindbom, Lennartpt_BR
dc.date.accessioned2020-07-09T21:22:47Z-
dc.date.available2020-07-09T21:22:47Z-
dc.date.issued2019pt_BR
dc.identifier.citationKenne E, Rasmuson J, Renné T, Vieira ML, Müller-Esterl W, Herwald H, et al. Neutrophils engage the kallikrein-kinin system to open up the endothelial barrier in acute inflammation. FASEB J. 2019 Jan;33(2):2599-2609. doi:10.1096/fj.201801329R.pt_BR
dc.identifier.urihttps://repositorio.butantan.gov.br/handle/butantan/2666-
dc.description.abstractNeutrophil recruitment and plasma exudation are key elements in the immune response to injury or infection. Activated neutrophils stimulate opening of the endothelial barrier; however, the underlying mechanisms have remained largely unknown. In this study, we identified a pivotal role of the proinflammatory kallikrein-kinin system and consequent formation of bradykinin in neutrophil-evoked vascular leak. In mouse and hamster models of acute inflammation, inhibitors of bradykinin generation, and signaling markedly reduced plasma exudation in response to chemoattractant activation of neutrophils. The neutrophil-driven leak was likewise suppressed in mice deficient in either the bradykinin B-2 receptor or factor XII (initiator of the kallikrein-kinin system). In human endothelial cell monolayers, material secreted from activated neutrophils induced cytoskeletal rearrangement, leading to paracellular gap formation in a bradykinin-dependent manner. As a mechanistic basis, we found that a neutrophil-derived heparin-binding protein (HBP/azurocidin) displaced the bradykinin precursor high-molecular-weight kininogen from endothelial cells, thereby enabling proteolytic processing of kininogen into bradykinin by neutrophil and plasma proteases. These data provide novel insight into the signaling pathway by which neutrophils open up the endothelial barrier and identify the kallikrein-kinin system as a target for therapeutic interventions in acute inflammatory reactions.Kenne, E., Rasmuson, J., Renne, T., Vieira, M. L., Muller-Esterl, W., Herwald, H., Lindbom, L. Neutrophils engage the kallikrein-kinin system to open up the endothelial barrier in acute inflammation.pt_BR
dc.description.sponsorshipSwedish Research Councilpt_BR
dc.description.sponsorshipSwedish Heart-Lung Foundationpt_BR
dc.description.sponsorshipTorsten Söderberg Foundationpt_BR
dc.description.sponsorship(SSF) Swedish Foundation for Strategic Researchpt_BR
dc.description.sponsorshipAlfred Österlunds Stiftelsept_BR
dc.description.sponsorshipGerman Research Societypt_BR
dc.description.sponsorshipEuropean Research Councilpt_BR
dc.description.sponsorshipKarolinska Institutetpt_BR
dc.format.extentp. 2599-2609pt_BR
dc.language.isoEnglishpt_BR
dc.relation.ispartofFASEB journalpt_BR
dc.titleNeutrophils engage the kallikrein-kinin system to open up the endothelial barrier in acute inflammationpt_BR
dc.typeArticlept_BR
dc.identifier.doi10.1096/fj.201801329Rpt_BR
dc.identifier.urlhttp://dx.doi.org/10.1096/fj.201801329Rpt_BR
dc.contributor.externalKarolinska Institutet¦¦Suéciapt_BR
dc.contributor.externalUniversity of Hamburg (UHH)¦¦Alemanhapt_BR
dc.contributor.externalLunds Universitet¦¦Suéciapt_BR
dc.contributor.externalGoethe University Frankfurt¦¦Alemanhapt_BR
dc.identifier.citationvolume33pt_BR
dc.identifier.citationissue2pt_BR
dc.subject.keywordvascular permeabilitypt_BR
dc.subject.keywordbradykininpt_BR
dc.subject.keywordleukocytept_BR
dc.subject.keyworddegranulationpt_BR
dc.relation.ispartofabbreviatedFASEB Jpt_BR
dc.identifier.citationabntv. 33, n. 2, p. 2599-2609, jan. 2019pt_BR
dc.identifier.citationvancouver2019 Jan;33(2):2599-2609pt_BR
dc.contributor.butantanVieira, Mônica Larucci|:Aluno|:Laboratório de Desenvolvimento de Vacinas:Centro de Biotecnologia|:pt_BR
dc.sponsorship.butantanAlfred Österlunds Stiftelse¦¦pt_BR
dc.sponsorship.butantanEuropean Research Council¦¦ERC-StG-2012-311575pt_BR
dc.sponsorship.butantanGerman Research Society¦¦SFB877pt_BR
dc.sponsorship.butantanKarolinska Institutet¦¦pt_BR
dc.sponsorship.butantanSwedish Foundation for Strategic Research (SSF)¦¦pt_BR
dc.sponsorship.butantanSwedish Heart-Lung Foundation¦¦pt_BR
dc.sponsorship.butantanSwedish Research Council¦¦pt_BR
dc.sponsorship.butantanTorsten Söderberg Foundation¦¦pt_BR
dc.identifier.bvsccBR78.1pt_BR
dc.identifier.bvsdbIBProdpt_BR
dc.description.dbindexedYespt_BR
item.openairetypeArticle-
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item.grantfulltextembargo_29990101-
item.languageiso639-1English-
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