Pharmacological strategies for targeting platelet activation in asthma. (June 2019)

• Record Type: Journal Article
• Authors: Pitchford, Simon; Cleary, Simon; Arkless, Kate; Amison, Richard
• Is Part Of: Current opinion in pharmacology. Volume 46(2019)
• Page Start: 55
• Page End: 64
• Publication Date: 2019-06
• Subjects: Pharmacology -- Periodicals; Pharmaceutical Preparations -- Periodicals; Drug Therapy -- Periodicals; Biopharmaceutics -- Periodicals; Pharmacologie -- Périodiques; Pharmacology; Periodicals; 615.105
• DOI: 10.1016/j.coph.2019.03.012
• Languages: English
• ISSNs: 1471-4892

Abstract

Highlights: Platelet activation is causal to the inflammatory responses in asthma. A dichotomy in platelet activation exists that separates functionalities in haemostasis to host defence and inflammation. Current anti-platelet drugs have been tested for anti-inflammatory actions in the context of asthma. New approaches targeting platelet activation applicable to inflammation might provide novel anti-platelet drugs for asthma. Abstract : The activation of platelets during host defence and inflammatory disorders has become increasingly documented. Clinical studies of patients with asthma reveal heightened platelet activation and accumulation into lung tissue. Accompanying studies in animal models of allergic lung inflammation, using protocols of experimentally induced thrombocytopenia proclaim an important role for platelets during the leukocyte recruitment cascade, tissue integrity, and lung function. The functions of platelets during these inflammatory events are clearly distinct to platelet functions during haemostasis and clot formation, and have led to the concept that a dichotomy (or polytomy, depending on what else platelets do) in platelet activation exists. The platelet, therefore, presents us with novel opportunities for modulating these inflammatory responses. This review discusses the rationale and effectiveness of current anti-platelet drugs in their use to supress inflammation with regard to asthma, and the need to consider novel possibilities for pharmacological modulation of platelet function associated with inflammation that are pharmacologically distinct to current anti-platelet therapies.