Resistance of Neisseria gonorrhoeae to non-oxidative killing by adherent human polymorphonuclear leucocytes.
Resistance of Neisseria gonorrhoeae to non-oxidative killing by adherent human polymorphonuclear leucocytes.
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DOI：
10.1111/j.1462-5822.2009.01308.x
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发表时间：
2009-07
影响因子：
3.4
通讯作者：
Seifert HS
中科院分区：
文献类型：
--
作者：
Criss AK;Katz BZ;Seifert HS
淋病奈瑟菌（Neisseria gonorrhoeae, Gc）的症状性感染以大量中性粒细胞（PMN）内流为特征，但PMN不能清除初始感染，表明Gc对PMN的攻击具有防御作用。在这项研究中，液体培养的Gc在同步感染粘附的白细胞介素8处理的人PMNs后存活。PMN暴露1小时后，FA1090 Gc存活40% ~ 70%，细菌数量增加。用细菌活力染料和大豆凝集素检测细胞外Gc的实验显示，细胞内和细胞外pmn相关Gc的一个子集都是可行的。在化学上或基因上缺乏产生活性氧（ROS）的PMNs中，Gc存活不受影响。这一结果甚至适用于刺激中性粒细胞ROS产生的OpaB+ Gc。过氧化氢酶和reca缺陷Gc对ROS更敏感，没有PMN存活缺陷。recN和ngo1686突变体Gc也表现出对ROS和PMNs的敏感性增加，但这些突变体在ROS缺陷细胞中无法存活。ngo1686突变体对细胞外PMN杀灭的敏感性增加，而对细胞内PMN杀灭的敏感性没有增加。我们得出结论，Gc对PMN的杀伤具有显著的抗性，杀伤独立于中性粒细胞ROS的产生，Ngo1686和RecN保护Gc免受非氧化性PMN抗菌因子的攻击。
Symptomatic infection with Neisseria gonorrhoeae (Gc) is characterized by abundant neutrophil (PMN) influx, but PMNs cannot clear initial infection, indicating Gc possess defenses against PMN challenge. In this study, survival of liquid-grown Gc was monitored after synchronous infection of adherent, interleukin 8-treated human PMNs. 40% to 70% of FA1090 Gc survived 1 h of PMN exposure, after which bacterial numbers increased. Assays with bacterial viability dyes along with soybean lectin to detect extracellular Gc revealed that a subset of both intracellular and extracellular PMN-associated Gc were viable. Gc survival was unaffected in PMNs chemically or genetically deficient for producing reactive oxygen species (ROS). This result held true even for OpaB+ Gc, which stimulate neutrophil ROS production. Catalase- and RecA-deficient Gc, which are more sensitive to ROS in vitro, had no PMN survival defect. recN and ngo1686 mutant Gc also exhibit increased sensitivity to ROS and PMNs, but survival of these mutants was not rescued in ROS-deficient cells. The ngo1686 mutant showed increased sensitivity to extracellular but not intracellular PMN killing. We conclude that Gc are remarkably resistant to PMN killing, killing occurs independently of neutrophil ROS production, and Ngo1686 and RecN defend Gc from non-oxidative PMN antimicrobial factors.
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