Peters, Mark John; (2001) The role of platelets in acute inflammation. Doctoral thesis (Ph.D), UCL (University College London).

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Abstract

Platelets are cell fragments with haemostatic and inflammatory properties which are present in huge numbers in the peripheral blood. Lung inflammation in the Acute Respiratory Distress Syndrome (ARDS) occurs with particular severity in pancytopenic patients who are receiving regular platelet transfusions. Histological and experimental evidence supports a role for platelets in the pathogenesis of this condition. This thesis is primarily concerned with the investigation of the role of platelets in the pathogenesis of vascular endothelial dysfunction in clinical severe inflammatory conditions such as ARDS and the more generalised Systemic Inflammatory Response Syndrome. An 18 month long prospective study of admissions to the Paediatric Intensive Care Unit (PICU) with ARDS was undertaken to determine the associations, clinical course and value of established severity markers of this and related conditions. Platelets from patients with ARDS and control PICU patients were analysed by flow cytometry to determine circulating levels of platelet activation. This study failed to demonstrate any differences in the two populations. A method was then developed to investigate the binding of platelets to other circulating inflammatory cells (predominantly neutrophils) as a means by which assessment of free platelet activation may underestimate the true extent of platelet activation. This method was subsequently used to investigate the properties of complexes of platelets and neutrophils with respect to adhesive, phagocytic and metabolic functions. Platelet neutrophil complexes were shown to represent activated sub-populations of both cell types. The capacity of platelets to interact with an established model of the vascular endothelium in culture was investigated by flow cytometry. Studies in intensive care patients and in adults with risk factors for cardiovascular disease indicated that levels of circulating platelet-neutrophil complexes may be related to the extent of endothelial activation.

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