Platelets stimulated by IgG-coated surfaces bind and activate neutrophils through a selectin-dependent pathway
2003 (English)In: Biomaterials, ISSN 0142-9612, E-ISSN 1878-5905, Vol. 24, no 9, 1559-1573 p.Article in journal (Refereed) Published
Blood platelets bind rapidly to foreign surfaces and interact with adsorbed proteins and neutrophil granulocytes. We demonstrate by use of luminol-amplified chemiluminescence under stirred and non-stirred conditions that platelets at IgG-coated surfaces amplify the neutrophil extracellular release of reactive oxygen species (ROS). The neutrophil response involved tyrosine phosphorylation, but was only in part induced by neutrophil Fcγ-receptor stimulation. The platelet mediated effects were contact-dependent since the respiratory burst was inhibited when the IgG-stimulated platelets were removed by filtration, but not when they were fixed in paraformaldehyde. Bodipyphallacidin-staining of filamentous actin (F-actin) revealed that an actin-dependent platelet adhesion supported the subsequent adhesion and spreading of neutrophils. The neutrophil ROS-response was lowered when the interaction between platelet P-selectin (CD62P) and neutrophil P-selectin glycoprotein ligand-l (PSGL-1 or CD162) was inhibited. The blocking of L-selectin (CD62L) or blocking of the interaction between platelet glycoprotein (Gp) IIb/IIIa and neutrophil complement receptor 3 (CR3) showed no effect. We conclude that platelet activation on immobilized IgG trigger a contact-dependent “frustrated” phagocytosis by neutrophils, associated with a release of toxic ROS.
Place, publisher, year, edition, pages
2003. Vol. 24, no 9, 1559-1573 p.
Medical and Health Sciences
IdentifiersURN: urn:nbn:se:liu:diva-26376DOI: 10.1016/S0142-9612(02)00543-4Local ID: 10910OAI: oai:DiVA.org:liu-26376DiVA: diva2:246925