Kubo A, Sasada M, Nishimura T, Moriguchi T, Kakita T, Yamamoto K, Uchino H
First Division of Internal Medicine, Faculty of Medicine, Kyoto University, Japan.
Clin Exp Immunol. 1987 Dec;70(3):658-63.
Oxygen radical generation was measured using peritoneal exudate polymorphonuclear leucocytes (PMN) from a strain of beige mice, an animal model of the Chediak-Higashi syndrome. These PMN have been shown to exhibit delayed microbial killing and impaired phagosome-lysosome fusion. The amount of superoxide anion released by the PMN of the beige mice was similar to that released by the PMN of the control mice. The PMN of beige mice generated slightly less hydrogen peroxide than the control. Hydroxyl radical (.OH) generation and luminol-dependent chemiluminescence were significantly lowered in beige PMN stimulated with opsonized zymosan (OZ) or phorbol myristate acetate (PMA). Cytochalasin B-treated beige PMN showed a decreased ability to degranulate myeloperoxidase in response to OZ or PMA. We demonstrated the significant decrease in .OH generation and chemiluminescence in beige PMN, which might be one of the reasons to explain delayed microbial killing.
使用来自一种米色小鼠品系(Chediak-Higashi综合征的动物模型)的腹膜渗出多形核白细胞(PMN)来测量氧自由基的产生。这些PMN已被证明表现出延迟的微生物杀伤和受损的吞噬体-溶酶体融合。米色小鼠的PMN释放的超氧阴离子量与对照小鼠的PMN释放的量相似。米色小鼠的PMN产生的过氧化氢比对照略少。在用调理酵母聚糖(OZ)或佛波醇肉豆蔻酸酯乙酸酯(PMA)刺激的米色PMN中,羟基自由基(·OH)的产生和鲁米诺依赖性化学发光显著降低。用细胞松弛素B处理的米色PMN对OZ或PMA的反应显示出脱颗粒髓过氧化物酶的能力下降。我们证明了米色PMN中·OH产生和化学发光的显著降低,这可能是解释微生物杀伤延迟的原因之一。