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
Neutrophils engage the kallikrein-kinin system to open up the endothelial barrier in acute inflammation
-
- Kenne, Ellinor (author)
- Karolinska Institutet,Karolinska Institute
-
- Rasmuson, Joel (author)
- Karolinska Institutet,Karolinska Institute
-
- Renné, Thomas (author)
- University Medical Center Hamburg-Eppendorf
- show more...
- show less...
- (creator_code:org_t)
- 2019
- 2019
- English 11 s.
- In: FASEB journal : official publication of the Federation of American Societies for Experimental Biology. - 1530-6860. ; 33:2, s. 2599-2609
- Journal article (peer-reviewed)
Abstract
Subject headings
Close
- 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
- MEDICIN OCH HÄLSOVETENSKAP -- Medicinska och farmaceutiska grundvetenskaper -- Cell- och molekylärbiologi (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Basic Medicine -- Cell and Molecular Biology (hsv//eng)
Keyword
- bradykinin
- degranulation
- leukocyte
- vascular permeability
Publication and Content Type
- art (subject category)
- ref (subject category)
Find in a library
- FASEB journal : official publication of the Federation of American Societies for... (Search for host publication in LIBRIS)
To the university's database
- 1 of 1
- Previous record
- Next record
- To hitlist
Find more in SwePub
- By the author/editor
- Kenne, Ellinor
- Rasmuson, Joel
- Renné, Thomas
- Vieira, Monica L ...
- Müller-Esterl, W ...
- Herwald, Heiko
- show more...
- Lindbom, Lennart
- show less...
- About the subject
-
- MEDICAL AND HEALTH SCIENCES
- MEDICAL AND HEAL ...
- and Basic Medicine
- and Cell and Molecul ...
- Articles in the publication
- FASEB journal : ...
- By the university
- Lund University
- Karolinska Institutet
Search outside SwePub
- Extend your search to:
- Google Book Search
- Google Scholar
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.
- Copyright © LIBRIS - National Library Systems
- LIBRIS.kb.se
