Leucocyte activation by collagen-stimulated platelets in whole blood
2002 (English)In: Scandinavian Journal of Clinical and Laboratory Investigation, ISSN 0036-5513, Vol. 62, no 6, 451-462 p.Article in journal (Refereed) Published
Interaction between vascular cells plays an important role in the initial phases of the inflammatory process, but the mechanisms responsible for cell-cell communication are not fully understood. In this study, activation of leucocytes and platelets in heparinized whole blood was assessed using lumi-aggregometry. This technique enables simultaneous measurement of aggregation and oxygen radical production by monitoring impedance and luminol-amplified chemiluminescence (CL), respectively. Collagen induced aggregation and CL, depending on dose, and markedly enhanced subsequent aggregation and CL-response triggered by the chemotactic peptide formyl-methionyl-leucyl-phenylalanine (fMet-Leu-Phe). Collagen stimulation of whole blood down- and upregulated the expression of L-selectin and CD11b, respectively. Monoclonal antibodies against sialyl LewisX and P-selectin caused a pronounced inhibition of the oxidative burst, triggered by collagen itself or by a combination of collagen and fMet-Leu-Phe. Furthermore, the Arg-Gly-Asp-Ser(RGDS)-peptide effectively inhibited collagentriggered aggregation and CL, and the subsequent enhancement of the fMet-Leu-Phe-induced responses. This suggests that fibrinogen plays a part in linking platelet GpIIb/IIIa with CD11b on the leucocyte surface. However, neither anti-CD11b nor the PI-peptide (containing the ?-chain motif in fibrinogen that interacts with CD11b) counteracted the stimulatory effects of activated platelets on leucocyte functions. The selectin- and integrin-antagonizing substances were ineffective on the CL-responses induced by fMet-Leu-Phe itself. This study suggests that, through selectin- and integrin-dependent interaction, activated platelets potentiate leucocyte aggregation and oxygen radical production, which might be important for the outcome of inflammatory reactions.
Place, publisher, year, edition, pages
2002. Vol. 62, no 6, 451-462 p.
Medical and Health Sciences
IdentifiersURN: urn:nbn:se:liu:diva-26382DOI: 10.1080/00365510260390000Local ID: 10916OAI: oai:DiVA.org:liu-26382DiVA: diva2:246931