Impact of Pro-Inflammatory Mediators on Agonist-Induced Platelet Activation

Abstract

Platelets are multi-functional cells which besides playing their role in hemostasis also contribute to immunity when activated via their immune receptors causing granule secretion, chemotaxis, and phagocytosis. All these immunological functions are pre hallmarks of platelets activation which can be enhanced by various pro-inflammatory mediators. In this study we investigated the role of different pro-inflammatory molecules on the priming of agonist-induced platelet aggregation responses. For this purpose, we employed several Pathogen/Damage associated molecular patterns (PAMP/DAMPS) like FMLP, glucose, FMLP treated blood cell’s supernatant, mitochondrial DNA (mtDNA) and mitochondrial proteins (mt proteins). We isolated platelets, manually counted them, and after treatment with a priming agent and stimulated with adenosine-diphosphate (ADP) and adrenaline (AD). Extent of aggregation was noted by using a time-lapse spectrophotometric assay. A notable aggregation of platelets in response to ADP and AD was found, and also a significant difference of aggregation between mtDNA primed group followed by adrenaline stimulation and only adrenaline treated group was observed. We surprisingly found no significant alteration in platelet aggregation profiles after pre-treatment with other priming agents (FMLP, Glucose, FMLP treated Blood cell’s lysate, Mitochondrial protein). In short, except mtDNA we unexpectedly did not find any remarkable effect of pro-inflammatory mediators on platelets aggregation, but this finding still requires more exploring regarding its incubation time and proinflammatory mediators’ concentrations. Key words: Hemostasis, Proinflammatory mediators, PAMPs, DAMPs, Immunity