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金黄色葡萄球菌 AraC 型调控因子 Rbf 对毒力因子 Hla 和酚可溶性调节蛋白 α 的转录调控。

Transcriptional regulation of virulence factors Hla and phenol-soluble modulins α by AraC-type regulator Rbf in Staphylococcus aureus.

机构信息

Department of Oncology, The First Affiliated Hospital, Division of Life Sciences and Medicine, University of Science and Technology of China. Anhui, Hefei 230027, China.

Department of Oncology, The First Affiliated Hospital, Division of Life Sciences and Medicine, University of Science and Technology of China. Anhui, Hefei 230027, China.

出版信息

Int J Med Microbiol. 2020 Jul;310(5):151436. doi: 10.1016/j.ijmm.2020.151436. Epub 2020 Jun 16.

Abstract

Staphylococcus aureus is a gram-positive pathogenic bacterium and is capable of secreting numerous toxins interfering directly with the host to cause acute infections. Rbf, a transcriptional regulator of AraC/XylS family, has been reported to promote biofilm formation in polysaccharide intercellular adhesion (PIA) mediated manner to cause chronic infections. In this study, we revealed the new virulence-mediated role of Rbf that can negatively regulate the hemolytic activity. Furthermore, Rbf can specifically bind to the hla and psmα promoters to repress their expression, resulting in significantly decreased production of phenol-soluble modulins α (PSMα) and alpha-toxin. Accordingly, the rbf mutant strain exhibited the increased pathogenicity compared to the wild-type (WT) strain in a mouse subcutaneous abscess model, representing a type of acute infection by S. aureus. Collectively, our results provide a novel insight into the virulence regulation and acute infections mediated by Rbf in S. aureus.

摘要

金黄色葡萄球菌是一种革兰氏阳性的致病细菌,能够分泌许多毒素,直接干扰宿主,导致急性感染。AraC/XylS 家族的转录调节因子 Rbf 已被报道通过多糖细胞间黏附素(PIA)介导的方式促进生物膜形成,从而导致慢性感染。在这项研究中,我们揭示了 Rbf 的新的毒力介导作用,它可以负调控溶血活性。此外,Rbf 可以特异性地结合 hla 和 psmα 启动子来抑制它们的表达,导致酚可溶性调节素α(PSMα)和α-毒素的产生显著减少。因此,与野生型(WT)菌株相比,rbf 突变株在小鼠皮下脓肿模型中表现出更高的致病性,代表了金黄色葡萄球菌引起的一种急性感染。总的来说,我们的研究结果为 Rbf 在金黄色葡萄球菌中的毒力调节和急性感染提供了新的见解。

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