Platelet Kinetics in Stable Asthmatic Patients

Taytard, A; Vuillemin, L

doi:10.1007/978-3-0348-7451-9_14

Cited by 8 publications

(10 citation statements)

References 2 publications

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“…Our results are of interest because platelet activation has recently been suggested to occur chiefly in allergic asthmatics, and increased platelet turnover (Gresele et al, 1987), reduced platelet survival time (Taytard et al, 1986) and prolonged bleeding times (Szczeklik et al, 1986) have all been found to be features of allergic asthma. However, such changes have not been observed consistently within the allergic population (Hemmendinger et al, 1989).…”

Section: Discussionmentioning

confidence: 64%

PAF‐induced bronchial hyperresponsiveness in the rabbit: contribution of platelets and airway smooth muscle

Coyle

Spina

Page

1990

British J Pharmacology

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Aerosol administration of platelet activating factor (PAF) to normal rabbits induced an enhanced airway responsiveness to inhaled histamine, 6 and 24 h after exposure. Following exposure to bovine serum albumin (BSA) as the carrier molecule for PAF, there was an increase in airway responsiveness to histamine 6h after challenge, although by 24 h this was not significantly different from the responsiveness of airways to histamine before BSA. PAF‐induced bronchial hyperresponsiveness at 24 h was associated with a substantial increase in the number of neutrophils and mononuclear cells and a small, but significant increase in the number of eosinophils in the lungs as assessed by bronchoalveolar lavage. BSA exposure failed to alter the total number of cells in the lungs, although there was a significant increase in the number of neutrophils in the bronchoalveolar lavage fluid. Selective platelet depletion with a guinea‐pig anti‐rabbit platelet serum inhibited PAF‐induced bronchial hyperresponsiveness. In addition, there was an attenuation of PAF‐induced airway inflammation in animals rendered thrombocytopenic. The contractile potency to histamine, methacholine and carbachol was similar in intrapulmonary bronchi taken from rabbits exposed to an aerosol of BSA or PAF. Furthermore, the relaxant potency to the non‐selective β‐adrenoceptor agonist isoprenaline, was unaltered in PAF‐treated rabbits. In contrast, there was a 2.58 fold reduction in the relaxant potency to theophylline in rabbits exposed to PAF compared with rabbits exposed to BSA. These results suggest that in the rabbit, PAF‐induced bronchial hyperresponsiveness at 24 h is associated with airways inflammation and is dependent upon platelet activation, but is not related to changes in airway smooth muscle function.

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Section: Discussionmentioning

confidence: 64%

PAF‐induced bronchial hyperresponsiveness in the rabbit: contribution of platelets and airway smooth muscle

Coyle

Spina

Page

1990

British J Pharmacology

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“…This accelerated platelet consumption correlates to a shortened time taken to regenerate the platelet population. These phenomena can be corrected by treatment of asthmatic patients with glucocorticoids, or platelets treated with di-sodium chromoglycate in vitro before re-infusion, although these anti-inflammatory drugs have no known direct affects on platelet activation (Taytard et al, 1985;Tunon-De-Lara et al, 1992).…”

Section: Platelet Activation In Asthma and Rhinitismentioning

confidence: 99%

Novel uses for anti‐platelet agents as anti‐inflammatory drugs

Pitchford

2007

British J Pharmacology

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An alteration in the character and function of platelets is manifested in patients with inflammatory diseases, and these alterations have been dissociated from the well‐characterized involvement of platelets in thrombosis and haemostasis. Recent evidence reveals platelet activation is sometimes critical in the development of inflammation. The mechanisms by which platelets participate in inflammation are diverse, and offer numerous opportunities for future drug intervention. There is now acceptance that platelets act as innate inflammatory cells in immune responses, with roles as sentinel cells undergoing surveillance, responding to microbial invasion, orchestrating leukocyte recruitment, and migrating through tissue, causing damage and influencing repair processes in chronic disease. Some of these processes are targeted by drugs that are being developed to target platelet participation in atherosclerosis. The actions of platelets therefore influence the pathogenesis of diverse inflammatory diseases in various body compartments, encompassing parasitic and bacterial infection, allergic inflammation (especially asthma and rhinitis), and non‐atopic inflammatory conditions, for example, chronic obstructive pulmonary disease (COPD), rheumatoid arthritis (RA), inflammatory bowel disease (IBD) and atherosclerosis. This review will first discuss the evidence for platelet activation in these various inflammatory diseases, and secondly discuss the mechanisms by which this pathogenesis occurs and the various anti‐platelet agents which have been developed to combat platelet activation in atherosclerosis and their potential future use for the treatment of other inflammatory diseases.British Journal of Pharmacology (2007) 152, 987–1002; doi:10.1038/sj.bjp.0707364; published online 2 July 2007

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“…Furthermore, an alteration in the lifespan of platelets has been reported in stable atopic asthmatic patients, decreasing from 8.9 days to 4.7 days, suggestive of continual platelet consumption as a result of chronic activation . It was also reported that treatment with corticosteroids improved platelet turnover, thus reversing the observed shortening of platelet lifespan in atopic asthmatic patients . In contradiction, other groups have reported no differences in platelet lifespan between healthy individuals and patients with asthma, or pulmonary platelet sequestration after allergen challenge, suggesting the mechanisms governing platelet production, transit and lifespan in the context of inflammatory disease are complex .…”

Section: Introductionmentioning

confidence: 99%

Platelets and allergic inflammation

Page

Pitchford

2014

Clin Experimental Allergy

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Irrefutable clinical evidence demonstrates the activation of platelets in allergic diseases, including asthma, allergic rhinitis, and eczema. Indeed, experimental models of allergic disease have now shown that platelets play a fundamental role in the tissue recruitment of leucocytes following exposure to allergens. Furthermore, the extravascular presence of platelets in lungs of patients with asthma, and in animal models of allergic lung inflammation suggests that platelets may also contribute directly to allergic inflammation, through alterations in lung function, or by modulating processes involved in airway wall remodelling. Despite significant platelet activation in patients with allergic diseases, it is of note that these patients have been described as having a mild haemostastic defect, rather than an increased incidence of thrombosis. This suggests a dichotomy exists in platelet activation during inflammation compared to haemostasis, and that hitherto undiscovered platelet activation pathways might be exploited to create novel anti-inflammatory therapies without affecting the critical function of platelets in haemostasis.

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Platelet Kinetics in Stable Asthmatic Patients

Cited by 8 publications

References 2 publications

PAF‐induced bronchial hyperresponsiveness in the rabbit: contribution of platelets and airway smooth muscle

PAF‐induced bronchial hyperresponsiveness in the rabbit: contribution of platelets and airway smooth muscle

Novel uses for anti‐platelet agents as anti‐inflammatory drugs

Platelets and allergic inflammation

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