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葡萄球菌中毒性休克综合征毒素-1与肠毒素A对人血单核细胞T细胞增殖及TNFα分泌的相互作用

Interaction of staphylococcal toxic shock syndrome toxin-1 and enterotoxin A on T cell proliferation and TNFα secretion in human blood mononuclear cells.

作者信息

De Boer M L, Kum W W, Chow A W

机构信息

Division of Infectious Diseases, Departments of Medicine.

出版信息

Can J Infect Dis. 1999 Nov;10(6):403-8. doi: 10.1155/1999/234876.

DOI:10.1155/1999/234876
PMID:22346398
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3250724/
Abstract

BACKGROUND

The majority of menstrual toxic shock syndrome (MTSS) cases are caused by a single clone of Staphylococcus aureus that produces both toxic shock syndrome toxin-1 (TSST-1) and staphylococcal enterotoxin A (SEA).

OBJECTIVE

To determine whether the two superantigens interact to cause an enhancement of biological activity in human peripheral blood mononuclear cells (PBMCs).

DESIGN

PBMCs from nine healthy donors were stimulated with TSST-1 or SEA, either alone or in combination at their minimum effective concentrations.

SETTING

In vitro study.

INTERVENTIONS

Human PBMCs were stimulated in vitro with TSST-1 (1 pg/mL), SEA (0.1 pg/mL) or combination for 20 to 72 h. Mitogenic response was determined by [(3)H]-thymidine incorporation. PBMC culture supernatants were assayed for the presence of tumour necrosis factor-alpha (TNFα), interleukin (IL)-1β and IL-6 by ELISA.

MAIN RESULTS

The combination of TSST-1 and SEA induced significantly greater mitogenesis in human PBMCs compared with either toxin alone (P<0.05, paired Student's t test, two-tailed). Similarly, the production of TNFα in culture supernatants was significantly greater in the combination of TSST-1 and SEA compared with either TSST-1 or SEA alone (P<0.05). In contrast, no enhancement in the levels IL-1 or IL-6 was observed.

CONCLUSIONS

These data suggest that the co-production of TSST-1 and SEA by S aureus may provide some biological advantage to the organism throughs an enhanced effect of these superantigens on T cell activation and TNF secretion.

摘要

背景

大多数月经中毒性休克综合征(MTSS)病例由单一克隆的金黄色葡萄球菌引起,该菌可产生中毒性休克综合征毒素-1(TSST-1)和葡萄球菌肠毒素A(SEA)。

目的

确定这两种超抗原是否相互作用,导致人外周血单核细胞(PBMC)的生物活性增强。

设计

来自9名健康供体的PBMC用TSST-1或SEA单独或联合以其最低有效浓度进行刺激。

设置

体外研究。

干预措施

人PBMC在体外分别用TSST-1(1 pg/mL)、SEA(0.1 pg/mL)或两者联合刺激20至72小时。通过[³H]-胸腺嘧啶核苷掺入法测定有丝分裂反应。用ELISA检测PBMC培养上清液中肿瘤坏死因子-α(TNFα)、白细胞介素(IL)-1β和IL-6的存在情况。

主要结果

与单独使用任何一种毒素相比,TSST-1和SEA联合使用在人PBMC中诱导的有丝分裂显著更强(P<0.05,配对双尾学生t检验)。同样,与单独使用TSST-1或SEA相比,TSST-1和SEA联合使用时培养上清液中TNFα的产生显著更多(P<0.05)。相比之下,未观察到IL-1或IL-6水平的升高。

结论

这些数据表明,金黄色葡萄球菌同时产生TSST-1和SEA可能通过增强这些超抗原对T细胞活化和TNF分泌的作用,为该生物体提供一些生物学优势。

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本文引用的文献

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Functional activity of staphylococcal enterotoxin A requires interactions with both the alpha and beta chains of HLA-DR.葡萄球菌肠毒素A的功能活性需要与HLA - DR的α链和β链都相互作用。
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Interactions between staphylococcal superantigens and MHC class II molecules.葡萄球菌超抗原与MHC II类分子之间的相互作用。
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Clinical spectrum of nonmenstrual toxic shock syndrome (TSS): comparison with menstrual TSS by multivariate discriminant analyses.非经期中毒性休克综合征(TSS)的临床谱:通过多变量判别分析与经期TSS进行比较。
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Pathogenesis of the toxic shock syndrome: T cell mediated lethal shock caused by the superantigen TSST-1.中毒性休克综合征的发病机制:由超抗原TSST-1引起的T细胞介导的致死性休克。
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Early activation events induced by the staphylococcal superantigen toxic shock syndrome toxin-1 in human peripheral blood monocytes.葡萄球菌超抗原中毒性休克综合征毒素-1在人外周血单核细胞中诱导的早期激活事件。
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HLA class II molecule-mediated signal transduction mechanism responsible for the expression of interleukin-1 beta and tumor necrosis factor-alpha genes induced by a staphylococcal superantigen.HLA II类分子介导的信号转导机制,该机制负责由葡萄球菌超抗原诱导的白细胞介素-1β和肿瘤坏死因子-α基因的表达。
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Improved purification and biologic activities of staphylococcal toxic shock syndrome toxin 1.金黄色葡萄球菌中毒性休克综合征毒素1的纯化及生物学活性增强
J Clin Microbiol. 1993 Oct;31(10):2654-60. doi: 10.1128/jcm.31.10.2654-2660.1993.
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Superantigen mediated shock: a cytokine release syndrome.超抗原介导的休克:一种细胞因子释放综合征。
Immunobiology. 1993 Nov;189(3-4):270-84. doi: 10.1016/S0171-2985(11)80362-1.
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T cell receptor-major histocompatibility complex class II interaction is required for the T cell response to bacterial superantigens.T细胞受体与主要组织相容性复合体II类分子的相互作用是T细胞对细菌超抗原产生应答所必需的。
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Production of tumour necrosis factors by human T cells stimulated by a superantigen, toxic shock syndrome toxin-1.超抗原中毒性休克综合征毒素-1刺激人T细胞产生肿瘤坏死因子
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