SwePub
Sök i LIBRIS databas

  Extended search

onr:"swepub:oai:lup.lub.lu.se:ba111682-c613-44e9-8322-f91b95dd4f7f"
 

Search: onr:"swepub:oai:lup.lub.lu.se:ba111682-c613-44e9-8322-f91b95dd4f7f" > Neutrophils engage ...

  • 1 of 1
  • Previous record
  • Next record
  •    To hitlist
  • Kenne, EllinorKarolinska Institutet,Karolinska Institute (author)

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

  • Article/chapterEnglish2019

Publisher, publication year, extent ...

  • 2019
  • 11 s.

Numbers

  • LIBRIS-ID:oai:lup.lub.lu.se:ba111682-c613-44e9-8322-f91b95dd4f7f
  • https://lup.lub.lu.se/record/ba111682-c613-44e9-8322-f91b95dd4f7fURI
  • https://doi.org/10.1096/fj.201801329RDOI
  • http://kipublications.ki.se/Default.aspx?queryparsed=id:140228883URI

Supplementary language notes

  • Language:English
  • Summary in:English

Part of subdatabase

Classification

  • Subject category:art swepub-publicationtype
  • Subject category:ref swepub-contenttype

Notes

  • Neutrophil 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 B2 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., Renné, T., Vieira, M. L., Müller-Esterl, W., Herwald, H., Lindbom, L. Neutrophils engage the kallikrein-kinin system to open up the endothelial barrier in acute inflammation.

Subject headings and genre

Added entries (persons, corporate bodies, meetings, titles ...)

  • Rasmuson, JoelKarolinska Institutet,Karolinska Institute (author)
  • Renné, ThomasUniversity Medical Center Hamburg-Eppendorf (author)
  • Vieira, Monica L.Karolinska Institute,Karolinska Institutet,Lund University,Lunds universitet,Infektionsmedicin,Sektion III,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Infection Medicine (BMC),Section III,Department of Clinical Sciences, Lund,Faculty of Medicine,Instituto Butantan(Swepub:lu)med-ml22 (author)
  • Müller-Esterl, WernerGoethe University (author)
  • Herwald, HeikoLund University,Lunds universitet,Host parasite interactions,Forskargrupper vid Lunds universitet,Lund University Research Groups(Swepub:lu)medk-hhe (author)
  • Lindbom, LennartKarolinska Institute (author)
  • Karolinska InstitutetKarolinska Institute (creator_code:org_t)

Related titles

  • In:FASEB journal : official publication of the Federation of American Societies for Experimental Biology33:2, s. 2599-26091530-6860

Internet link

Find in a library

To the university's database

  • 1 of 1
  • Previous record
  • Next record
  •    To hitlist

Search outside SwePub

Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.

 
pil uppåt Close

Copy and save the link in order to return to this view