title: Aspirin treatment influences platelet-related inflammatory biomarkers in healthy individuals but not in acute stroke patients.
abstract: OBJECTIVE
  Platelet-leukocyte aggregation is believed to contribute to acute thrombotic events. While the effect of aspirin on platelet-to-platelet aggregation is well established, the impact of the drug on pro-inflammatory platelet function remains equivocal. Thus we investigated the effect of aspirin on selected platelet-related inflammatory biomarkers in both acute ischaemic stroke patients and healthy volunteers.
  
  
  METHODS
  Using five-colour flow cytometry the platelet surface expression of CD62P and CD40L and subpopulations of leukocyte-platelet aggregates were assessed in 63 acute stroke patients and 40 healthy volunteers at baseline and after a 10-day period of aspirin intake at a daily dose of 150 mg. Simultaneously the plasma levels of soluble CD62P and CD40L, serum level of TxB(2), and whole blood impedance platelet aggregation under arachidonic acid (AA) stimulation were investigated.
  
  
  RESULTS
  No differences in values of studied platelet-related inflammatory biomarkers in both resting platelets and those activated with TRAP after 10-day treatment with aspirin were confirmed in stroke subjects. In healthy individuals the resting platelet expression of CD62P, plasma level of soluble CD62P and percentage of circulating monocyte-platelet aggregates were lower after the aspirin intake period (P=0.009; P=0.04; P=0.004, respectively). In both studied groups serum level of TxB(2) and platelet aggregation under AA stimulation were lower than before treatment (P<0.001).
  
  
  CONCLUSIONS
  Despite effective inhibition of COX-1-dependent platelet aggregation, aspirin does not influence the platelet α-granule-derived inflammatory mediators and monocyte-platelet aggregation in acute stroke subjects, although it does in healthy individuals.
authors.affiliation: Department of Neurology, Poznan University of Medical Sciences, Poznan, Poland. mlukasik@ump.edu.pl
authors.forename: Maria
authors.initials: M
authors.lastname: Lukasik
authors.forename: Grzegorz
authors.initials: G
authors.lastname: Dworacki
authors.forename: Slawomir
authors.initials: S
authors.lastname: Michalak
authors.forename: Joanna
authors.initials: J
authors.lastname: Kufel-Grabowska
authors.forename: Jacek
authors.initials: J
authors.lastname: Golanski
authors.forename: Cezary
authors.initials: C
authors.lastname: Watala
authors.forename: Wojciech
authors.initials: W
authors.lastname: Kozubski
mesh_terms: D000368:Aged; D001241:Aspirin / Q000494:pharmacology*; D015415:Biomarkers / Q000097:blood; D001792:Blood Platelets / Q000187:drug effects / Q000473:pathology*; D023201:CD40 Ligand / Q000032:analysis; D016022:Case-Control Studies; D051545:Cyclooxygenase 1; D005260:Female; D005434:Flow Cytometry / Q000379:methods; D006801:Humans; D007249:Inflammation / Q000097:blood* / Q000188:drug therapy; D008297:Male; D008875:Middle Aged; D009000:Monocytes; D019007:P-Selectin / Q000032:analysis; D010973:Platelet Adhesiveness; D010975:Platelet Aggregation Inhibitors; D020521:Stroke / Q000097:blood*; D013929:Thromboxane B2 / Q000032:analysis
chemical_list: D015415:Biomarkers; D019007:P-Selectin; D010975:Platelet Aggregation Inhibitors; D023201:CD40 Ligand; D013929:Thromboxane B2; D051545:Cyclooxygenase 1; D001241:Aspirin