Render M L, Rounds S
Pulmonary Center, Boston University School of Medicine, Massachusetts.
Am Rev Respir Dis. 1988 Nov;138(5):1115-23. doi: 10.1164/ajrccm/138.5.1115.
The adherence of neutrophils (PMN) to endothelium is a crucial early step in neutrophil-mediated vascular injury. However, vascular injury is not a necessary event in inflammatory states, which suggests that endogenous mechanisms may protect endothelial cells from neutrophil-mediated injury. Previous studies suggested that leukocytes adhered in greater numbers to vascular endothelium in vivo and in vitro, where the contiguity of the cells was disrupted and where endothelial cells were actively migrating and proliferating. We studied the effect of development of a confluent monolayer on adherence of human PMN to cultured bovine calf aortic endothelial cells and investigated several mechanisms by which this effect might occur. We found that adherence of quiescent and activated PMN decreased with development of a confluent endothelial cell monolayer. A similar effect was found using human umbilical-vein endothelial cells. In contrast, adherence of nylon wool-nonadherent, thymus-derived lymphocytes increased. Variation in neutrophil adherence was not due to adherence of PMN to exposed tissue culture plastic or to exposed matrix components in preconfluent cultures, nor due to products released into culture supernatants. Diminished PMN adherence to postconfluent monolayers may have been related to changes in endothelial cell glycoproteins because neuraminidase or cycloheximide pretreatment augmented PMN adherence to postconfluent cultures more than to preconfluent cultures. However, the extent of total cell surface sialation, as assessed by neuraminidase-releasable [3H]glucosamine from metabolically labeled monolayers, did not differ between pre- and postconfluent cultures, suggesting that some specific sialated cell surface constituent is responsible for decreased PMN adherence to postconfluent monolayers.(ABSTRACT TRUNCATED AT 250 WORDS)
中性粒细胞（PMN）与内皮细胞的黏附是中性粒细胞介导的血管损伤中至关重要的早期步骤。然而，在炎症状态下血管损伤并非必然发生，这表明内源性机制可能保护内皮细胞免受中性粒细胞介导的损伤。先前的研究表明，在体内和体外，白细胞更多地黏附于血管内皮，此时细胞的连续性被破坏，内皮细胞处于活跃的迁移和增殖状态。我们研究了汇合单层的形成对人PMN黏附于培养的小牛主动脉内皮细胞的影响，并探讨了这种影响可能发生的几种机制。我们发现，随着汇合内皮细胞单层的形成，静止和活化的PMN的黏附减少。使用人脐静脉内皮细胞也发现了类似的效果。相反，尼龙毛非黏附性胸腺来源淋巴细胞的黏附增加。中性粒细胞黏附的变化并非由于PMN黏附于暴露的组织培养塑料或预汇合培养物中暴露的基质成分，也不是由于释放到培养上清液中的产物。PMN对汇合后单层的黏附减少可能与内皮细胞糖蛋白的变化有关，因为神经氨酸酶或环己酰亚胺预处理对PMN黏附于汇合后培养物的增强作用比对预汇合培养物的增强作用更大。然而，通过神经氨酸酶可释放的[3H]葡糖胺（来自代谢标记的单层）评估的总细胞表面唾液酸化程度在预汇合和汇合后培养物之间并无差异，这表明某些特定的唾液酸化细胞表面成分导致PMN对汇合后单层的黏附减少。（摘要截断于250字）
