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RNAIII抑制肽(RIP)可抑制agr调控的毒素产生。

RNAIII inhibiting peptide (RIP) inhibits agr-regulated toxin production.

作者信息

Vieira-da-Motta O, Ribeiro P D, Dias da Silva W, Medina-Acosta E

机构信息

Laboratório de Biologia do Reconhecer, Universidade Estadual do Norte Fluminense, Norte Fluminense, Brazil.

出版信息

Peptides. 2001 Oct;22(10):1621-7. doi: 10.1016/s0196-9781(01)00497-1.

DOI:10.1016/s0196-9781(01)00497-1
PMID:11587790
Abstract

Staphylococcal enterotoxins (SEs) are emetic toxins that cause food poisoning. SEs also function as powerful pyrogenic toxin superantigens that stimulate non-specific T-cell proliferation. Together with the hemolysins, SEs have been largely implicated as virulence factors in multiple infection models. Recent biochemical and genetic analyses have demonstrated that production of some of these toxins is partially regulated by quorum sensing mechanisms where proteins and peptides activate the accessory gene regulator (agr). Because toxin production is central to bacterial pathogenesis, therapeutic strategies alternative to antibiotics, and based on rational interference of the quorum sensing systems involved, are currently being developed. This approach would lead to repression of toxin production and, thus, to disease prevention. Here we provide evidence to conclude that synthetic analogs of the RNAIII inhibiting peptide (RIP) and antibodies to its target molecule TRAP function in vitro as efficient suppressors of agr-regulated exotoxin production by Staphylococcus aureus.

摘要

葡萄球菌肠毒素(SEs)是引起食物中毒的呕吐毒素。SEs还作为强大的致热毒素超抗原发挥作用,刺激非特异性T细胞增殖。与溶血素一起,SEs在多种感染模型中被很大程度地认为是毒力因子。最近的生化和基因分析表明,其中一些毒素的产生部分受群体感应机制调节,在该机制中蛋白质和肽激活辅助基因调节因子(agr)。由于毒素产生是细菌发病机制的核心,目前正在开发基于合理干扰相关群体感应系统的抗生素替代治疗策略。这种方法将导致毒素产生受到抑制,从而预防疾病。在此我们提供证据得出结论,RNAIII抑制肽(RIP)的合成类似物及其靶分子TRAP的抗体在体外作为金黄色葡萄球菌agr调节的外毒素产生的有效抑制剂发挥作用。

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