What is it about?
In acute inflammation, neutrophil activation is known to stimulate vascular hyperpermeability and consequent leakage of plasma into tissue. However, underlying mechanisms have remained obscure. We demonstrate that neutrophil-derived granule proteins act in synergy to initiate proteolysis of endothelial-bound high molecular weight kininogen leading to local generation of bradykinin which in turn triggers endothelial cell contraction and gap formation.
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Why is it important?
Our data provide novel insight into the paracellular signaling by which neutrophils stimulate opening of the endothelial barrier and will help to refine therapeutic strategies in order to manage destructive hyperpermeability in the host response to injury or infection.
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This page is a summary of: Neutrophils engage the kallikrein‐kinin system to open up the endothelial barrier in acute inflammation, The FASEB Journal, October 2018, Wiley,
DOI: 10.1096/fj.201801329r.
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