Changes in phagocyte activity in patients with ischaemic stroke

Abstract

The activity of peripheral phagocytes to generate reactive oxygen species (ROS) was studied in healthy individuals and patients with ischaemic stroke. The aim was to clarify the relationship between phagocyte activity, the time elapsed after the onset of disease and stroke severity. The total and extracellular production of ROS were evaluated by luminol chemiluminescence. Simultaneously the plasma oxidant activity was determined. When stimulated by opsonized zymosan, phagocytes in patients with stroke (regardless of its severity) showed fast activation. The total ROS generation increased over time in all stroke cases studied. However, the extracellular ROS generation was found to be greater in patients with severe stroke than in those with mild neurological deficiency. When stimulated by formyl-methionyl-leucyl-phenylalanine, the total oxidative phagocyte capacity (regardless of stroke severity) increased over time, but there was no change in the amount of extracellularly generated ROS. In patients with stroke the oxidant activity of plasma was enhanced. We conclude that circulating phagocytes in patients with ischaemic stroke are primed for enhanced ROS production by opsonin receptor-mediated stimulation and for increased secretion of myeloperoxidase by opsonin receptor-independent stimulation. The enhanced extracellular generation of ROS through opsonin receptor-dependent stimulation may be considered an oxidative stress biomarker in cerebral ischaemia.

Oxidative stress in the chronic phase after stroke

“…5 Extracellular ROS generation was found to correlate with the clinical outcome of patients and the size of the hypodense area. It is also known that phagocytes in acute stroke are able to be activated on attachment to the vascular endothelium with subsequent generation of toxic oxygen products and extracellular release of potentially destructive proteases.…”

“…[2][3][4] Data have been published showing altered leukocyte rheology and ability to generate ROS, correlating with the severity of neurological deficits and clinical outcome. 5,6 A change in blood antioxidant capacity and oxidative membrane damage in patients with acute stroke also has been reported. [7][8][9][10] According to the National Institute of Neurological Disorders and Stroke (USA), 25% of people who recover from their first stroke will have another stroke within 5 years.…”

“…To compare LCL responses of different individuals at different moments in the chronic stroke phase, the data for S were normalized with respect to total phagocyte count and RBC absorption in the blood samples. 5,17 The number of phagocytes comprises polymorphonuclear phagocytes, eosinophils and monocytes and was determined by the white blood cell count minus lymphocytes.…”

Oxidative stress in brain aging, neurodegenerative and vascular diseases: An overview

“…It has also been estimated that up to 30% of all ischemic strokes will eventually undergo hemorrhagic transformation. Brain ischemia, and especially the condition of ischemia and reperfusion occurring after stroke, has been shown to be associated with free radical-mediated reactions potentially leading to neuronal death [135].…”

The Parkinson's disease gene DJ-1 is also a key regulator of stroke-induced damage

“…It is caused by the interruption of the brain blood supply due to occlusion (ischemic) or rupture of blood vessels (hemorrhagic) leading to neuronal dysfunction and death. Although, the complete nature of the complex intra-/extracellular signals that regulate neuronal injury remains to be clarified, a growing body of evidence supports the essential role of oxidative stress in initiation and progression of the injury process (3,4).…”