Densen P, Mandell G L
J Clin Invest. 1978 Dec;62(6):1161-71. doi: 10.1172/JCI109235.
Gonococci are capable of attaching to the surface of polymorphonuclear leukocytes (PMN). In this location they resist phagocytosis and are not killed by PMN. To delineate the factors involved in the survival of these gonococci, we investigated the interaction of virulent gonococci, which adhere to cells and resist phagocytosis, and avirulent gonococci, which are phagocytized and killed by PMN. In the presence of serum, both virulent and avirulent gonococci associate equally well with PMN and stimulate increases in oxidative metabolism. In the absence of serum virulent gonococci attached to PMN and stimulated PMN oxidative metabolism to a greater extent than avirulent gonococci which did not attach to PMN (P = 0.0009). Therefore, the survival of virulent gonococci attached to the PMN surface is not a result of failure to activate oxidative and bactericidal mechanisms. Both virulent and avirulent gonococci stimulated equivalent PMN specific granule release as measured by the appearance of lactoferrin in the media. Phagocytosis of avirulent gonococci stimulated significantly greater beta-glucuronidase release (P = 0.01) and myeloperoxidase-mediated iodination of protein (P = 0.001) by PMN than attachment of virulent gonococci. In the absence of serum neither type of gonococci stimulated beta-glocuronidase release or protein iodination by PMN. Thus, virulent gonococci fail to stimulate primary granule release by PMN. To further assess the role of attachment versus ingestion on the survival of gonococci, PMN were treated with cytochalasin B to block ingestion. Cytochalasin B-treated PMN were unable to kill either virulent or avirulent gonococci despite normal degranulation stimulated by the latter. The failure of PMN to kill surface-attached gonococci appears to be a consequence of the failure of PMN to enclose the virulent gonococci within a phagosome. The phagocytic vacuole thus plays a critical role in normal PMN bactericidal activity by providing a closed space in which the proper concentration of substances may be achieved to generate microbicidal activity.
淋球菌能够附着在多形核白细胞（PMN）表面。在此位置，它们能抵抗吞噬作用，不会被PMN杀死。为了阐明这些淋球菌存活所涉及的因素，我们研究了有毒力的淋球菌（能黏附于细胞并抵抗吞噬作用）与无毒力的淋球菌（会被PMN吞噬并杀死）之间的相互作用。在有血清存在的情况下，有毒力和无毒力的淋球菌与PMN的结合情况相同，并刺激氧化代谢增加。在无血清时，黏附于PMN的有毒力淋球菌比未黏附于PMN的无毒力淋球菌更能刺激PMN的氧化代谢（P = 0.0009）。因此，附着于PMN表面的有毒力淋球菌的存活并非由于未能激活氧化和杀菌机制。通过检测培养基中乳铁蛋白的出现情况可知，有毒力和无毒力的淋球菌刺激PMN特异性颗粒释放的程度相当。与有毒力淋球菌的黏附相比，无毒力淋球菌的吞噬显著刺激了PMN释放更多的β-葡萄糖醛酸酶（P = 0.01）以及髓过氧化物酶介导的蛋白质碘化作用（P = 0.001）。在无血清时，两种类型的淋球菌均未刺激PMN释放β-葡萄糖醛酸酶或进行蛋白质碘化。因此，有毒力的淋球菌无法刺激PMN释放初级颗粒。为了进一步评估黏附与吞噬对淋球菌存活的作用，用细胞松弛素B处理PMN以阻断吞噬作用。尽管细胞松弛素B处理的PMN能被无毒力淋球菌正常刺激脱颗粒，但它们无法杀死有毒力或无毒力的淋球菌。PMN无法杀死表面附着的淋球菌似乎是由于PMN未能将有毒力的淋球菌包裹在吞噬小体内。吞噬泡通过提供一个封闭空间，在其中可达到产生杀菌活性所需的物质适当浓度，从而在正常PMN杀菌活性中发挥关键作用。
