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首页> 外文期刊>Journal of Molecular Biology >Role of Phenol-Soluble Modulins in Staphylococcus epidermidis Biofilm Formation and Infection of Indwelling Medical Devices
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Role of Phenol-Soluble Modulins in Staphylococcus epidermidis Biofilm Formation and Infection of Indwelling Medical Devices

机译：苯酚 - 可溶性调节蛋白在葡萄球菌的作用的作用生物膜形成和感染留置医疗装置

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摘要

Phenol-soluble modulins (PSMs) are amphipathic, alpha-helical peptides that are secreted by staphylococci in high amounts in a quorum-sensing-controlled fashion. Studies performed predominantly in Staphylococcus aureus showed that PSMs structure biofilms, which results in reduced biofilm mass, while it has also been reported that S. aureus PSMs stabilize biofilms due to amyloid formation. We here analyzed the roles of PSMs in in vitro and in vivo biofilms of Staphylococcus epidermidis, the leading cause of indwelling device-associated biofilm infection. We produced isogenic deletion mutants for every S. epidermidis psm locus and a sequential deletion mutant in which production of all PSMs was abolished. In vitro analysis substantiated the role of all PSMs in biofilm structuring. PSM-dependent biofilm expansion was not observed, in accordance with our finding that no S. epidermidis PSM produced amyloids. In a mouse model of indwelling device-associated infection, the total psm deletion mutant had a significant defect in dissemination. Notably, the total psm mutant produced a significantly more substantial biofilm on the implanted catheter than the wild-type strain. Our study, which for the first time directly quantified the impact of PSMs on biofilm expansion on an implanted device, shows that the in vivo biofilm infection phenotype in S. epidermidis is in accordance with the PSM biofilm structuring and detachment model, which has important implications for the potential therapeutic application of quorum-sensing blockers.
机译：苯酚可溶性调节蛋白（PSMS）是两栖酸性的α-螺旋肽，其通过质量传感控制的时尚高量的葡萄球菌分泌。主要在金黄色葡萄球菌中进行的研究表明，PSMS结构生物膜，这导致生物膜质量降低，同时还据报道了由于淀粉样蛋白形成而稳定生物膜的S.UUREUS PSM。我们在这里分析了PSM在体外和体内生物膜的角色，葡萄球菌表皮体体内，是留置装置相关的生物膜感染的主要原因。对于每种S.表皮蛋白轨迹和序贯缺失突变体产生了同源缺失突变体，其中废除了所有PSM的生产。体外分析证实了所有PSM在生物膜结构中的作用。根据我们的发现，没有观察到PSM依赖的生物膜扩张，没有S.表皮蛋白PSM产生淀粉样蛋白。在留置设备相关感染的小鼠模型中，总PSM删除突变体具有显着的缺陷。值得注意的是，PSM总突变体在植入的导管上产生了比野生型菌株在植入的导管上产生显着更大的生物膜。我们的研究是，首次直接量化PSM对植入装置上的生物膜扩张的影响，表明，S.表皮的体内生物膜感染表型符合PSM生物膜结构和分离模型，具有重要意义对于频压传感阻滞剂的潜在治疗应用。

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