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• W2147661805 abstract "In humans, heparin-binding protein (HBP) and the potent chemotactic lipid leukotriene B(4) (LTB(4)) are important mediators of innate immune responses. Here we show that human neutrophils (PMNs) challenged with LTB(4) (30 s to 5 min) release HBP as determined by Western blot analysis. This response peaks at 100 nM of agonist and is mediated by the BLT1 receptor. Protein phosphatase-1 (30 microM) and wortmannin (0.5 microM) block the LTB(4)-mediated HBP release from PMNs, which suggests involvement of the 1-phosphatidylinositol 3-kinase intracellular pathway during degranulation. Furthermore, postsecretory supernatants from LTB(4)-stimulated PMNs induce intracellular calcium mobilization in endothelial cells in vitro and increase in vascular permeability in vivo, as assessed in a mouse model of pleurisy. Selective removal of HBP from the supernatant significantly reduces these activities attributing a key role to HBP in the LTB(4)-induced change in vascular permeability. This lipid-protein axis could offer novel opportunities for pharmacological intervention in key steps of the vascular response to inflammation." @default.
• W2147661805 created "2016-06-24" @default.
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• W2147661805 date "2009-01-16" @default.
• W2147661805 modified "2023-10-07" @default.
• W2147661805 title "Leukotriene B₄‐ induced changes in vascular permeability are mediated by neutrophil release of heparin‐binding protein (HBP/CAP37/azurocidin)" @default.
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• W2147661805 doi "https://doi.org/10.1096/fj.08-121277" @default.
• W2147661805 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19151333" @default.
• W2147661805 hasPublicationYear "2009" @default.
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