Abstract
Neutrophils have been observed rolling along the luminal surface of endothelium in small venules (Atherton and Born, 1972, 1973; Fiebig et al., 1991; Ley et al., 1989, 1991a). In the early stages of acute inflammation this phenomenon is markedly increased (House and Lipowsky, 1987; Zimmerman and Granger, 1990; Kubes et al., 1990; Hernandez et al., 1987), and the rolling cells frequently stop, change shape, and emigrate into the surrounding tissue. Arfors et al., (1987) initially raised the possibility that the mechanisms accounting for the rolling phenomenon are different from those causing stationary adhesion and emigration. They observed, in a study on the effects of anti-CD 18 monoclonal antibody 60.3 in a rabbit model of inflammation, that the systemic administration of this antibody prevented neutrophils from stopping and transmigrating, but the rolling behavior of these cells was apparently unaffected. Lawrence et al., (1990) used a parallel plate flow chamber in vitro to stimulate some of the forces affecting neutrophil adhesion to endothelial cells, and assessed the ability of isolated neutrophils to adhere while flowing past a confluent monolayer of human umbilical vein endothelial cells (HUVEC). They demonstrated that in this flow system, few neutrophils interacted with the HUVEC monolayer even at wall shear stresses much lower than those predicted to occur in vivo.
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Abbassi, O., Jones, D., Mariscalco, M., McEver, R., McIntire, L.V., Wayne Smith, C. (1994). Effects of Shear Stress on Leukocyte Adhesion. In: Metcalf, B.W., Dalton, B.J., Poste, G., Schatz, J. (eds) Cellular Adhesion. New Horizons in Therapeutics. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-2466-3_8
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