Pharmacological modulation of the inflammatory actions of platelets.
Patients with inflammatory diseases often exhibit a change in platelet function, with these alterations being clearly distinct from the well-characterized role of platelets in haemostasis and thrombosis. It has recently been revealed that platelets can behave as innate inflammatory cells in immune responses with roles in leukocyte recruitment, migration into tissues, release of cytotoxic mediators, and in tissue remodelling following injury.Platelets exhibit a wide range of receptors for mediators involved in the inflammatory pathway and the immune response (Fig. 1). These include purinergic receptors, selectins, integrins, toll-like receptors, immunoglobulins, and chemokine receptors, but the precise role platelets play in the inflammatory process is still under investigation. Nevertheless, given that many of these receptors are distinct from those involved in thrombosis and haemostasis, this raises the real possibility of targeting these receptors to regulate inflammatory diseases without compromising haemostasis.
Sackler Institute of Pulmonary Pharmacology, King's College London, 150 Stamford Street, Room 5.44, 5th Floor, Franklin-Wilkins Building, Waterloo Campus, London, SE1 9NH, UK.
Richard
R
Amison
Clive
C
Page
Simon
S
Pitchford
D000818:Animals; D001792:Blood Platelets / Q000187:drug effects* / Q000502:physiology; D000077144:Clopidogrel; D006801:Humans; D007249:Inflammation / Q000188:drug therapy*; D016328:NF-kappa B / Q000502:physiology; D015539:Platelet Activation; D010973:Platelet Adhesiveness / Q000187:drug effects; D013988:Ticlopidine / Q000031:analogs & derivatives / Q000494:pharmacology
D016328:NF-kappa B; D000077144:Clopidogrel; D013988:Ticlopidine