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Article type: Research Article
Authors: Pitzer, J.E.a | Del Zoppo, G.J.b | Schmid-Schönbein, G.W.a; *
Affiliations: [a] Department of Bioengineering and Institute for Biomedical Engineering, University of California, San Diego, La Jolla, CA 92093-0412, USA | [b] Department of Molecular and Experimental Medicine, The Scripps Research Institute, 10666 North Torrey Pines Road, La Jolla, CA 92037, USA
Correspondence: [*] Correspondence: G. W. Schmid-Schönbein, Department of Bioengineering and Institute for Biomedical Engineering, University of California, San Diego, La Jolla, CA 92093-0412, USA; Tel.: (619) 534-3852; Fax: (619) 534-5722
Abstract: Smoking and elevated leukocyte counts are risk factors for cardiovascular disease. Experimental studies suggest that leukocyte activation may be a requirement for certain cardiovascular complications. Clinical studies have demonstrated activated leukocytes in the peripheral blood of stroke victims. Accordingly, neutrophil activation in unseparated whole blood of smokers as well as naive neutrophils of non-smokers exposed to plasma of smokers was investigated. Both spontaneous superoxide formation as determined by nitroblue tetrazolium reduction, as well as pseudopod formation, are significantly elevated in autologous neutrophils of smokers. The surface expression of CD18 and L-selectin on autologous circulating neutrophils of smokers is not significantly different from non-smoker controls. In contrast, incubation of naive neutrophils with smoker plasma leads to significantly higher levels of superoxide formation, pseudopod formation, and L-selectin shedding, compared with non-smoker plasma, suggesting that the plasma of smokers contains a transferable factor which causes leukocyte activation. The results indicate that analysis of blood samples from large peripheral veins may not accurately reflect leukocyte activation in the circulation since activated leukocytes have a higher probability to be trapped in the microcirculation.
Keywords: Adhesion, selectin, integrin, superoxide, actin, pseudopod formation, organ injury
DOI: 10.3233/BIR-1996-33104
Journal: Biorheology, vol. 33, no. 1, pp. 45-58, 1996
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