Effects of shear stress on adhesive interaction between neutrophils and cultured endothelial cells

• Published in: Journal of applied physiology (1985) Vol. 63; no. 5; p. 2031
• Main Authors: Worthen, G S, Smedly, L A, Tonnesen, M G, Ellis, D, Voelkel, N F, Reeves, J T, Henson, P M
• Format: Journal Article
• Language: English
• Published: United States 01-11-1987
• Subjects: 6-Ketoprostaglandin F1 alpha - pharmacology; Animals; Cattle; Cell Adhesion - drug effects; Cells, Cultured; Endothelium, Vascular - physiology; Microscopy, Electron; Neutrophils - drug effects; Neutrophils - physiology; Plastics; Pulmonary Artery - physiology; Stress, Mechanical; Viscosity; Zymosan - pharmacology
• ISSN: 8750-7587
• DOI: 10.1152/jappl.1987.63.5.2031

The effect of hydrodynamic shear stress on the adhesive interaction between neutrophils and endothelial cells in vitro was investigated using an apparatus similar to a cone-in-plate viscometer. Isolated bovine neutrophils were labeled with 111In and incubated with monolayers of cultured bovine pulmonary arterial endothelial cells in the presence of different degrees of shear stress. Physiologically relevant shear (less than 2 dyn/cm2) was associated with marked decrease in neutrophil adherence. Stimulation with 10% bovine zymosan-activated plasma increased adherence under static conditions but failed to increase adherence conducted during the application of shear stress. Inhibition of endothelial cell prostacyclin production by meclofenamate or aspirin failed to alter the response to shear. Incubation of neutrophils under static conditions for 10, but not 5, min however, markedly enhanced subsequent resistance to shear, suggesting that a time-dependent reaction between neutrophil and endothelial cell was required to induce an increase in the strength of adherence. Analysis of neutrophil migration underneath the monolayer indicated that such migration in no way accounted for resistance to shear, particularly since shear resistance was enhanced on serum-coated plastic as well as endothelial cells. We conclude that hemodynamic factors may play an important role in modulating neutrophil adherence to endothelium in both normal and inflammatory states.