Rest R F, Frangipane J V
Department of Microbiology, Hahnemann University School of Medicine, Philadelphia, Pennsylvania 19102-1192.
Infect Immun. 1992 Mar;60(3):989-97. doi: 10.1128/iai.60.3.989-997.1992.
Gonococci possessing certain opacity-associated (Opa) outer membrane proteins adhere to and are phagocytosed by human neutrophils in the absence of serum. Recently, it has been shown that serum-sensitive strains of Neisseria gonorrhoeae possessing the appropriate lipooligosaccharide phenotype become serum resistant when grown in the presence of CMP-N-acetylneuraminic acid (CMP-NANA) because of sialylation of their lipooligosaccharide. We investigated whether such sialylation affects nonopsonic (antibody- and complement-independent) interactions of gonococci with human neutrophils in vitro. We grew Opa+ gonococci in the presence of up to 50 micrograms of CMP-NANA per ml, incubated them with neutrophils in vitro, and measured their abilities to adhere to neutrophils, stimulate neutrophil luminol-dependent chemiluminescence (LDCL), and be phagocytically killed by neutrophils. Growth in CMP-NANA dramatically inhibited (in a dose-dependent manner) the ability of Opa+ gonococci to adhere to neutrophils and stimulate neutrophil LDCL. Growth of Opa+ gonococci in 50 micrograms of CMP-NANA per ml appeared to delay, but did not inhibit, their killing by neutrophils. Sialidase treatment of sialylated Opa+ gonococci, i.e., gonococci grown with CMP-NANA, totally restored their abilities to adhere to neutrophils and stimulate neutrophil LDCL. Opa- gonococci grown in the presence of 50 micrograms of CMP-NANA per ml and opsonized with fresh human serum bound to neutrophils only about 30% less efficiently than did Opa- gonococci grown without CMP-NANA and opsonized. The results of our studies show that sialylated Opa+ gonococci have dramatically reduced nonopsonic interactions with neutrophils. Some gonococcal strains may resist killing by human neutrophils in vivo by such a mechanism.
在无血清的情况下，具有某些不透明相关（Opa）外膜蛋白的淋球菌可黏附并被人中性粒细胞吞噬。最近有研究表明，具有合适脂寡糖表型的淋病奈瑟菌血清敏感菌株，在CMP-N-乙酰神经氨酸（CMP-NANA）存在的情况下生长时，由于其脂寡糖的唾液酸化作用而变得具有血清抗性。我们研究了这种唾液酸化作用是否会影响淋球菌与人类中性粒细胞在体外的非调理（不依赖抗体和补体）相互作用。我们在每毫升高达50微克CMP-NANA存在的情况下培养Opa⁺淋球菌，将它们与中性粒细胞在体外孵育，并测量它们黏附于中性粒细胞、刺激中性粒细胞鲁米诺依赖性化学发光（LDCL）以及被中性粒细胞吞噬杀灭的能力。在CMP-NANA中生长显著抑制（呈剂量依赖性）Opa⁺淋球菌黏附于中性粒细胞并刺激中性粒细胞LDCL的能力。每毫升含有50微克CMP-NANA的情况下培养Opa⁺淋球菌，似乎会延迟但不会抑制它们被中性粒细胞杀灭。用唾液酸酶处理经唾液酸化的Opa⁺淋球菌，即与CMP-NANA一起生长的淋球菌，可完全恢复它们黏附于中性粒细胞并刺激中性粒细胞LDCL的能力。每毫升含有50微克CMP-NANA的情况下培养的Opa⁻淋球菌，并用新鲜人血清进行调理，其与中性粒细胞结合的效率仅比未用CMP-NANA培养并调理的Opa⁻淋球菌低约30%。我们的研究结果表明，经唾液酸化的Opa⁺淋球菌与中性粒细胞的非调理相互作用显著减少。一些淋球菌菌株可能通过这种机制在体内抵抗被人类中性粒细胞杀灭。
