LFA‐1/ICAM‐3 mediates neutrophil homotypic aggregation under fluid shear stress

We found that human neutrophils undergo homotypic aggregation by loading the physiological range of fluid shear stress (12–30 dynes/cm2). Under the fluid shear stress, an increase of intracellular Ca2+ concentration of neutrophils was observed. This increase of intracellular Ca2+ concentration was caused by Ca2+ influx, and the blockage of the flux by NiCl2 suppressed the neutrophil homotypic aggregation. Furthermore, this neutrophil aggregation under fluid shear stress was completely inhibited by pretreatment with antibody against LFA‐1 or ICAM‐3. These results suggested that NiCl2‐sensitive Ca2+ channel played an important role in LFA‐1/ICAM‐3‐mediated neutrophil homotypic aggregation under fluid shear stress. © 1996 Wiley‐Liss, Inc.

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