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Microbial interactions and differential protein expression in Staphylococcus aureus –Candida albicans dual-species biofilms

机译:金黄色葡萄球菌-白色念珠菌双物种生物膜中的微生物相互作用和差异蛋白表达

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摘要

The fungal species Candida albicans and the bacterial species Staphylococcus aureus are responsible for a majority of hospital-acquired infections and often coinfect critically ill patients as complicating polymicrobial biofilms. To investigate biofilm structure during polymicrobial growth, dual-species biofilms were imaged with confocal scanning laser microscopy. Analyses revealed a unique biofilm architecture where S. aureus commonly associated with the hyphal elements of C. albicans. This physical interaction may provide staphylococci with an invasion strategy because candidal hyphae can penetrate through epithelial layers. To further understand the molecular mechanisms possibly responsible for previously demonstrated amplified virulence during coinfection, protein expression studies were undertaken. Differential in-gel electrophoresis identified a total of 27 proteins to be significantly differentially produced by these organisms during coculture biofilm growth. Among the upregulated staphylococcal proteins was l-lactate dehydrogenase 1, which confers resistance to host-derived oxidative stressors. Among the downregulated proteins was the global transcriptional repressor of virulence factors, CodY. These findings demonstrate that the hyphae-mediated enhanced pathogenesis of S. aureus may not only be due to physical interactions but can also be attributed to the differential regulation of specific virulence factors induced during polymicrobial growth. Further characterization of the intricate interaction between these pathogens at the molecular level is warranted, as it may aid in the design of novel therapeutic strategies aimed at combating fungal–bacterial polymicrobial infection.
机译:真菌种类的白色念珠菌和细菌种类的金黄色葡萄球菌是造成大多数医院获得性感染的原因,并且通常使重症患者并发感染,使微生物生物膜复杂化。为了研究微生物生长过程中的生物膜结构,用共聚焦扫描激光显微镜对双物种生物膜成像。分析揭示了独特的生物膜结构,其中金黄色葡萄球菌通常与白色念珠菌的菌丝成分相关。这种物理相互作用可以为葡萄球菌提供入侵策略,因为念珠菌丝可以穿透上皮层。为了进一步了解可能导致先前证明的共感染期间扩增的毒力的分子机制,进行了蛋白质表达研究。差异凝胶电泳确定共27种蛋白质在共培养生物膜生长过程中由这些生物体显着差异产生。在上调的葡萄球菌蛋白中有l-乳酸脱氢酶1,它赋予了对宿主衍生的氧化应激源的抗性。在下调的蛋白质中,有毒力因子CodY的全局转录阻遏物。这些发现表明,金黄色葡萄球菌的菌丝介导的发病机理增强不仅可能是由于物理相互作用,而且还可以归因于在微生物生长过程中诱导的特定毒力因子的差异调节。这些病原体之间在分子水平上的复杂相互作用的进一步表征是有必要的,因为它可能有助于设计旨在对抗真菌-细菌多微生物感染的新型治疗策略。

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