Lack of an Increased Expression of the CD11b/CD18 Antigen on the Surface of Peripheral Blood Circulating Pool of Leukocytes in Patients with an Acute Neurological Ischemic Event
OBJECTIVE: To reveal the intensity of the surface expression of the adhesion molecules (CD11b/CD18) on monocytes and neutrophils in the peripheral blood of patients with an acute brain ischemia compared to healthy individuals who served as controls. BACKGROUND: The Leukocyte Integrin CD11b/CD18 is an important receptor that is involved in the modulation of leukocyte to endothelial interactions and is expressed in increased amounts during cell activation. It has been previously suggested that activated white blood cells, mainly polymorphonuclear leukocytes and monocytes, participate in the development of ischemic vascular disorders by virtue of their capability to obstruct the microvasculature and enhance tissue damage. DESIGN/METHODS: Cellular surface expression of the adhesion molecules CD11b/CD18 on the neutrophils and monocytes in the peripheral blood was measured by a direct immunotechnique of flow cytometry in two groups: patients who had transient ischemic attacks (TIA) or ischemic stroke (confirmed by CT scans, within 24 hours from onset of symptoms), and healthy individuals who served as controls. Analysis was done by ANOVA test. RESULT: Seventy-one patients and 150 controls were included in the study. The respective mean fluorescence intensity for CD11b/CD18 being 161±76, 155±87 for polymorphonuclear leukocytes and 231±99, 203±79 for monocytes. No statistically significant difference was noted between the groups. CONCLUSIONS: The results of the present study show that patients with acute cerebral ischemic event do not present increased amount of the CD11b/CD18 antigen on the surface of the peripheral blood polymorphonuclear or monocytes compared to control. Our data do not support the hypothesis that the white blood cells participate in the development of acute cerebral ischemia by the mechanism of activation of the adhesion molecule CD11b/CD18.