E-SELECTIN SUPPORTS NEUTROPHIL ROLLING IN-VITRO UNDER CONDITIONS OF FLOW
E-SELECTIN SUPPORTS NEUTROPHIL ROLLING IN-VITRO UNDER CONDITIONS OF FLOW
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DOI：
10.1172/jci116889
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发表时间：
1993-12-01
影响因子：
15.9
通讯作者：
SMITH, CW
中科院分区：
文献类型：
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作者：
ABBASSI, O;KISHIMOTO, TK;SMITH, CW
评价E-选择素在流动条件下支持中性粒细胞粘附的能力。在1.85达因/厘米2的壁剪切应力，中性粒细胞被发现附着到E-选择素的L细胞单层的顶面上表达。最初的细胞间接触最常见的证据是中性粒细胞滚动的单层上的平均速率一致，以10 μ m/s。抗E-选择素单克隆抗体CL 2/6抑制这种相互作用> 90%。滚动的中性粒细胞经常短暂停止，但与刺激的内皮细胞的行为相反，它们保持球形形状，并且不在单层上或单层下迁移。中性粒细胞L-选择素对这种相互作用的可能贡献由以下发现指示：抗L-选择素单克隆抗体DREG-56在流动下抑制E-选择素依赖性粘附> 65%，并且在流动下L-选择素和E-选择素依赖性粘附的表面水平之间存在高度显著的相关性。在流动条件下，E-选择素似乎也支持中性粒细胞粘附于IL-1 β刺激的内皮细胞，但它仅占粘附水平的30%，而L-选择素则占> 65%。因此，L-选择素和E-选择素都可以在壁剪切应力下支持中性粒细胞粘附，从而阻止细胞间粘附分子-1依赖性粘附，并且它们在流动条件下参与中性粒细胞粘附到刺激的内皮细胞。
E-selectin was evaluated for its ability to support neutrophil adhesion under conditions of flow. At a wall shear stress of 1.85 dyn/cm2, neutrophils were found to attach to E-selectin expressed on the apical surface of L cell monolayers. The initial intercellular contact was most often evidenced by neutrophils rolling on the monolayer at a mean rate of congruent-to 10 mum/s. Anti-E-selectin monoclonal antibody, CL2/6, inhibited this interaction by > 90%. Rolling neutrophils often transiently stopped, but in contrast to the behavior on stimulated endothelial cells, they remained spherical in shape and did not migrate on or beneath the monolayer. A possible contribution of neutrophil L-selectin to this interaction was indicated by the findings that anti-L-selectin monoclonal antibody, DREG-56, inhibited E-selectin-dependent adhesion under flow by > 65%, and there was a highly significant correlation between surface levels of L-selectin and E-selectin-dependent adhesion under flow. E-selectin also appeared to support neutrophil adhesion to IL-1beta-stimulated endothelial cells under conditions of flow, but it accounted for only congruent-to 30% of the level of adherence, in contrast to L-selectin which accounted for > 65%. Thus, both L-selectin and E-selectin can support neutrophil adhesion at wall shear stresses that preclude intercellular adhesion molecule-1-dependent adhesion, and they participate in neutrophil adherence to stimulated endothelial cells under conditions of flow.