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蛋白II+淋球菌对人白细胞的刺激是由凝集素样淋球菌成分介导的。

Stimulation of human leukocytes by protein II+ gonococci is mediated by lectin-like gonococcal components.

作者信息

Rest R F, Lee N, Bowden C

出版信息

Infect Immun. 1985 Oct;50(1):116-22. doi: 10.1128/iai.50.1.116-122.1985.

Abstract

We investigated the ability of carbohydrates, glycosidases, and concanavalin A to inhibit the stimulation of the human leukocyte oxidative burst by gonococci in the absence of serum. The gonococci used in this study contained protein II (P.II) outer membrane proteins, and neutrophil oxidative burst was measured by luminol-enhanced chemiluminescence (CL). The following carbohydrates inhibited CL induced by nonpiliated P.II+ gonococci: beta-D-glucosamine greater than N-acetylneuraminic acid (sialic acid) greater than mannose greater than alpha-methylmannoside greater than N-acetyl-beta-D-glucosamine greater than or equal to glucose greater than or equal to lactose. Fucose, galactose, or beta-D-galactosamine (all 100 mM) did not inhibit or slightly increased CL, indicating a specificity for the observed effects. Mannose and alpha-methylmannoside also inhibited induction of monocyte CL by P.II+ gonococci. Incubation of neutrophils with concanavalin A inhibited subsequent gonococcus-induced CL but not phorbol myristate acetate-induced CL. Treatment of neutrophils with alpha-mannosidase reduced subsequent gonococcus-induced CL greater than 99%, whereas such treatment of gonococci had no effect on their ability to induce neutrophil CL. Incubation of a P.IIb-containing variant of Neisseria gonorrhoeae FA1090 with anti-P.IIb monoclonal antibody inhibited subsequent stimulation of neutrophil CL in a dose-responsive manner, indicating a specific role for P.IIb in the stimulatory process. The data suggest that one or more lectin-like components on the surface of P.II+ gonococci mediate their ability to stimulate the oxidative burst of human phagocytes.

摘要

我们研究了在无血清条件下,碳水化合物、糖苷酶和伴刀豆球蛋白A抑制淋球菌刺激人白细胞氧化爆发的能力。本研究中使用的淋球菌含有蛋白II(P.II)外膜蛋白,通过鲁米诺增强化学发光法(CL)测定中性粒细胞的氧化爆发。以下碳水化合物可抑制非菌毛P.II⁺淋球菌诱导的CL:β-D-葡糖胺>N-乙酰神经氨酸(唾液酸)>甘露糖>α-甲基甘露糖苷>N-乙酰-β-D-葡糖胺≥葡萄糖≥乳糖。岩藻糖、半乳糖或β-D-半乳糖胺(均为100 mM)不抑制或轻微增加CL,表明所观察到的效应具有特异性。甘露糖和α-甲基甘露糖苷也可抑制P.II⁺淋球菌诱导的单核细胞CL。用伴刀豆球蛋白A孵育中性粒细胞可抑制随后淋球菌诱导的CL,但不抑制佛波酯诱导的CL。用α-甘露糖苷酶处理中性粒细胞可使随后淋球菌诱导的CL降低99%以上,而用该酶处理淋球菌对其诱导中性粒细胞CL的能力没有影响。用抗P.IIb单克隆抗体孵育淋病奈瑟菌FA1090的含P.IIb变体,以剂量反应方式抑制随后对中性粒细胞CL的刺激,表明P.IIb在刺激过程中起特定作用。数据表明,P.II⁺淋球菌表面的一种或多种凝集素样成分介导了它们刺激人吞噬细胞氧化爆发的能力。

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本文引用的文献

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The pathology of gonorrhoea.淋病的病理学
Br J Vener Dis. 1948 Dec;24(4):137-47.
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Colony opacity and protein II compositions of gonococci.淋球菌的菌落透明度和蛋白II组成
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