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Neutrophil activation in smokers
Affiliation:1. Schroeder Institute for Tobacco Research and Policy Studies, Legacy, Washington, DC, USA;2. Department of Health, Behavior, and Society, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA;3. Gillings School of Public Health, University of North Carolina, Chapel Hill, NC, USA;4. Department of Research and Evaluation, Legacy, Washington, DC, USA;5. Department of Oncology, Georgetown Lombardi Comprehensive Cancer Center, USA;6. Westat, Rockville, MD, USA;7. Institute for Health Research and Policy, University of Illinois at Chicago, USA
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 CD 18 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.
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