Daniels I, Crouch S P, Lindsay M A, Morgan A G, Burden R P, Fletcher J
Medical Research Centre, City Hospital, Nottingham, United Kingdom.
Clin Diagn Lab Immunol. 1994 Mar;1(2):227-31. doi: 10.1128/cdli.1.2.227-231.1994.
Peritoneal dialysis effluent from patients with end-stage renal failure contains a low-molecular-weight solute that inhibits the killing of phagocytosed Staphylococcus epidermidis by polymorphonuclear leukocytes (PMN). This observation has been investigated by using luciginen-enhanced chemiluminescence to measure PMN NADPH oxidase activity, CD11b/CD18 expression and lactoferrin release to measure secondary granule discharge, and cellular levels of beta-glucuronidase (EC 3.2.1.31) to measure changes in primary granules. Peritoneal dialysis effluent had no effect on the loss of intracellular beta-glucuronidase from normal unstimulated PMN or from PMN stimulated with S. epidermidis. It did, however, cause a concentration-dependent (0 to 70%; vol/vol) increase in expression of CD11b/CD18 and NADPH oxidase activity. CD11b/CD18 expression increased over 20 min before starting to plateau. Release of lactoferrin by the same cells demonstrated a strong positive correlation with integrin expression (P < 0.001, Spearman's rank correlation coefficient). When dialysis effluent-treated PMN were stimulated with formyl-methionylleucylphenylalanine, integrin expression, release of lactoferrin, and NADPH oxidase activity were greater than in PMN treated with formyl-methionylleucylphenylalanine alone. Under these conditions, a concentration-dependent increase in CD11b/ CD18 and lactoferrin release were observed only at a concentration between 0 and 30% (vol/vol) dialysis effluent, while a concentration-dependent increase in oxidase activity was seen at a concentration between 0 and 70% (vol/vol). The results suggest that dialysis effluent does not affect PMN primary granule release but does cause increased release of secondary granules and an increase in NADPH oxidase activity in both unstimulated and stimulated PMN.
终末期肾衰竭患者的腹膜透析流出液含有一种低分子量溶质，它会抑制多形核白细胞（PMN）对吞噬的表皮葡萄球菌的杀伤作用。通过使用鲁米诺增强化学发光法来测量PMN的NADPH氧化酶活性、CD11b/CD18表达以及乳铁蛋白释放以测量次级颗粒释放，并通过测量β-葡萄糖醛酸酶（EC 3.2.1.31）的细胞水平来测量初级颗粒的变化，对这一观察结果进行了研究。腹膜透析流出液对正常未刺激的PMN或经表皮葡萄球菌刺激的PMN中细胞内β-葡萄糖醛酸酶的损失没有影响。然而，它确实导致CD11b/CD18表达和NADPH氧化酶活性呈浓度依赖性（0至70%；体积/体积）增加。CD11b/CD18表达在开始达到平稳之前的20分钟内增加。同一细胞释放的乳铁蛋白与整合素表达呈强正相关（P < 0.001，Spearman等级相关系数）。当用甲酰甲硫氨酰亮氨酰苯丙氨酸刺激经透析流出液处理的PMN时，整合素表达、乳铁蛋白释放和NADPH氧化酶活性均高于仅用甲酰甲硫氨酰亮氨酰苯丙氨酸处理的PMN。在这些条件下，仅在透析流出液浓度为0至30%（体积/体积）时观察到CD11b/CD18和乳铁蛋白释放呈浓度依赖性增加，而在透析流出液浓度为0至70%（体积/体积）时观察到氧化酶活性呈浓度依赖性增加。结果表明，透析流出液不影响PMN初级颗粒的释放，但确实会导致未刺激和刺激的PMN中次级颗粒释放增加以及NADPH氧化酶活性增加。
