Marcinkiewicz J, Czajkowska B, Grabowska A, Kasprowicz A, Kociszewska B
Department of Immunology, Jagiellonian University Medical College, Cracow, Poland.
Immunology. 1994 Dec;83(4):611-6.
Activated rodent macrophages produce high amounts of nitric oxide (NO). NO as a tumoricidal and defence molecule against intracellular parasites is commonly accepted. However, its role as an obligatory killing factor for extracellular bacteria is controversial. In the present study we stimulated murine peritoneal macrophages by heat-killed bacteria (Staphylococcus aureus, S. epidermidis and Escherichia coli). In some groups bacteria were pretreated with HOCl, to replace the chlorinating system in activated neutrophils that operates as a bactericidal system in vivo. High levels of NO, tumour necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) were detected after stimulation by all non-chlorinated bacteria strains tested. However, after chlorination Gram-positive bacteria lost their ability to induce NO and TNF-alpha, whereas phagocytosis and IL-6 production were not affected by chlorination.
活化的啮齿动物巨噬细胞会产生大量一氧化氮（NO）。NO作为一种针对细胞内寄生虫的杀肿瘤和防御分子已被广泛认可。然而，其作为细胞外细菌的必需杀伤因子的作用存在争议。在本研究中，我们用热灭活的细菌（金黄色葡萄球菌、表皮葡萄球菌和大肠杆菌）刺激小鼠腹腔巨噬细胞。在一些组中，细菌用次氯酸（HOCl）预处理，以替代活化中性粒细胞中的氯化系统，该系统在体内作为杀菌系统发挥作用。在所测试的所有未氯化细菌菌株刺激后，均检测到高水平的NO、肿瘤坏死因子-α（TNF-α）和白细胞介素-6（IL-6）。然而，氯化后革兰氏阳性菌失去了诱导NO和TNF-α的能力，而吞噬作用和IL-6的产生不受氯化影响。
