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Titel: Microvascular Mechanisms of Polyphosphate-Induced Neutrophil-Endothelial Cell Interactions in vivo
VerfasserIn: Du, Feifei
Wang, Yongzhi
Ding, Zhiyi
Laschke, Matthias W.
Thorlacius, Henrik
Sprache: Englisch
Titel: European Surgical Research
Bandnummer: 60
Heft: 1-2
Seiten: 53-62
Verlag/Plattform: Karger
Erscheinungsjahr: 2019
Freie Schlagwörter: Endothelium
Inflammation
Leukocyte
Transmigration
DDC-Sachgruppe: 610 Medizin, Gesundheit
Dokumenttyp: Journalartikel / Zeitschriftenartikel
Abstract: Background: Polyphosphates (PolyPs) have been reported to exert pro-inflammatory effects. However, the molecular mechanisms regulating PolyP-provoked tissue accumulation of leukocytes are not known. The aim of the present investigation was to determine the role of specific adhesion molecules in PolyP-mediated leukocyte recruitment. Methods: PolyPs and TNF-α were intrascrotally administered, and anti-P-selectin, anti-E-selectin, anti-P-selectin glycoprotein ligand-1 (PSGL-1), anti-membrane-activated complex-1 (Mac-1), antilymphocyte function antigen-1 (LFA-1), and neutrophil depletion antibodies were injected intravenously or intraperitoneally. Intravital microscopy of the mouse cremaster microcirculation was used to examine leukocyte-endothelium interactions and recruitment in vivo. Results: Intrascrotal injection of PolyPs increased leukocyte accumulation. Depletion of neutrophils abolished PolyP-induced leukocyte-endothelium interactions, indicating that neutrophils were the main leukocyte subtype responding to PolyP challenge. Immunoneutralization of P-selectin and PSGL-1 abolished PolyP-provoked neutrophil rolling, adhesion, and emigration. Moreover, immunoneutralization of Mac-1 and LFA-1 had no impact on neutrophil rolling but markedly reduced neutrophil adhesion and emigration evoked by PolyPs. Conclusion: These results suggest that P-selectin and PSGL-1 exert important roles in PolyP-induced inflammatory cell recruitment by mediating neutrophil rolling. In addition, our data show that Mac-1 and LFA-1 are necessary for supporting PolyP-triggered firm adhesion of neutrophils to microvascular endothelium. These novel findings define specific molecules as potential targets for pharmacological intervention in PolyP-dependent inflammatory diseases.
DOI der Erstveröffentlichung: 10.1159/000497435
URL der Erstveröffentlichung: https://doi.org/10.1159/000497435
Link zu diesem Datensatz: urn:nbn:de:bsz:291--ds-441697
hdl:20.500.11880/39503
http://dx.doi.org/10.22028/D291-44169
ISSN: 1421-9921
0014-312X
Datum des Eintrags: 28-Jan-2025
Fakultät: M - Medizinische Fakultät
Fachrichtung: M - Chirurgie
Professur: M - Prof. Dr. Michael D. Menger
Sammlung:SciDok - Der Wissenschaftsserver der Universität des Saarlandes

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