Modulating influence of chemotactic factor-induced cell adhesiveness on granulocyte function.
Modulating influence of chemotactic factor-induced cell adhesiveness on granulocyte function.
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趋化因子诱导的细胞粘附性对粒细胞功能的调节影响。
DOI：
10.1172/jci109466
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发表时间：
1979
期刊：
影响因子：
--
通讯作者：
C. Dahinden
中科院分区：
文献类型：
--
作者：
J. Fehr;C. Dahinden
粘附在调节多形核白细胞（PMN）的运动和积累的重要性仍然是模糊的。我们发现重悬于热灭活血浆中的人PMN的趋化性在1-10 nM N-甲酰-甲硫氨酸-亮氨酸-苯丙氨酸（f-Met-Leu-Phe）时最大，但在>/= 100 nM时低于随机运动性。这种令人印象深刻的运动性降低被培养皿上的细胞粘附增加所抵消，在1 nM时最小，在>10 nM f-Met-Leu-Phe时最大（分别为6+/-1和37+/-2% [SE]粘附细胞）。相差显微镜观察发现，受刺激粘附的细胞失去了运动PMN的典型双极形状，变得固定和高度扁平。PMN，预先暴露于250 nM的f-Met-Leu-Phe和洗涤后测试，保留增加的粘附性，并显示出极低的随机和趋化运动。相比之下，预先暴露于1 nM f-Met-Leu-Phe对趋化性没有影响。支持的概念，即固定hyperplasia不对应于一个一般的功能性低反应的PMN，没有抑郁症的初始摄取率的存在下，观察到250 nM的f-Met-Leu-Phe。此外，发现PMN活化的诱导与己糖单磷酸途径活性的刺激以及溶酶体酶释放的刺激之间存在密切的相关性（r >/= 0.98）。因此，N-甲酰肽的“趋化性失活”和“高剂量趋化性抑制”是细胞增殖增加的结果。这种现象为炎症部位的细胞捕获提供了机制。相反，如果在循环血液中起作用，例如，在败血症中，它可能损害PMN向这些部位迁移。
The importance of adhesion in regulating locomotion and accumulation of polymorphonuclear leukocytes (PMN) has remained vague. We found that the chemotaxis of human PMN resuspended in heat-inactivated plasma was maximal toward 1-10 nM N-formyl-met-leu-phe (f-Met-Leu-Phe), but fell below random motility toward >/= 100 nM. This impressive decrease of motility was paralleled by increased cell adherence on Petri dishes being minimal at 1 nM and maximal at >10 nM f-Met-Leu-Phe (6+/-1 and 37+/-2% [SE] adherent cells, respectively). Checked by phase-contrast microscopy, cells under stimulated adhesion lost the typical bipolar shape of moving PMN and became immobilized and highly flattened. PMN, preexposed to 250 nM f-Met-Leu-Phe and tested after washing, retained increased adhesiveness and showed extremely low random and chemotactic motility. In contrast, preexposure to 1 nM f-Met-Leu-Phe had no effect on chemotaxis. Supporting the concept that immobilizing hyperadhesiveness does not correspond to a general functional hyporesponsiveness of PMN, no depression of the initial ingestion rate was observed in the presence of 250 nM f-Met-Leu-Phe. Moreover, a close correlation was found between the induction of PMN adhesiveness and the stimulation of the hexose monophosphate pathway activity as well as of lysomal enzyme release (r >/= 0.98). Thus, "chemotactic deactivation" and "high-dose inhibition of chemotaxis" by N-formyl peptides is the consequence of increased cell adhesiveness. This phenomenon provides a mechanism for cell trapping at the inflammatory site. Conversely, if operative in circulating blood, e.g., in septicemia, it may impair PMN emigration to such sites.