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Blood, 15 September 2007, Vol. 110, No. 6, pp. 1879-1886.
Prepublished online as a Blood First Edition Paper on June 4, 2007; DOI 10.1182/blood-2006-08-040980.
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Submitted August 15, 2006
Accepted May 27, 2007
Conversion of platelets from a pro-aggregatory to a pro-inflammatory adhesive phenotype: role of PAF in spatially regulating neutrophil adhesion and spreading
Suhasini Kulkarni, Kevin J Woollard, Stephen Thomas, David Oxley, and Shaun P Jackson*
Australian Centre for Blood Diseases, Monash University, & the Baker Heart Research Institute, at Alfred Medical Research & Education Precinct, Melbourne, Victoria, Australia
The National Institute for Biological Standards and Control, Potters Bar, United Kingdom
Proteomic Research Group, The Babraham Institute, Cambridge, United Kingdom
* Corresponding author; email: shaun.jackson{at}med.monash.edu.au.
The ability of platelets to provide a highly reactive surface for the recruitment of other platelets and leukocytes to sites of vascular injury is critical for hemostasis, atherothrombosis and a variety of inflammatory diseases. The mechanisms co-ordinating platelet-platelet and platelet-leukocyte interactions have been well defined and in general, it is assumed that increased platelet activation correlates with enhanced reactivity towards other platelets and neutrophils. In the current study, we demonstrate a differential role for platelets in supporting platelet and neutrophil adhesive interactions under flow. We demonstrate that the conversion of spread platelets to microvesiculated procoagulant (annexin A5 +ve) forms reduces platelet-platelet adhesion and leads to a paradoxical increase in neutrophil-platelet interaction. This enhancement in neutrophil adhesion and spreading is partially mediated by the pro-inflammatory lipid, platelet activating factor (PAF). PAF production, unlike other neutrophil chemokines (IL-8, GRO- , NAP-2, IL-1 ) is specifically and markedly upregulated in annexin A5 +ve cells. Physiologically, this spatially-controlled production of PAF plays an important role in localizing neutrophils on the surface of thrombi. These studies define for the first time a specific pro-inflammatory function for annexin A5 +ve platelets. Moreover, they demonstrate an important role for platelet-derived PAF in spatially regulating neutrophil adhesion under flow.
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