Peters Brian M, Jabra-Rizk Mary Ann, Scheper Mark A, Leid Jeff G, Costerton John William, Shirtliff Mark E
Graduate Program in Life Sciences, Molecular Microbiology and Immunology Program, University of Maryland - Baltimore, Baltimore, MD, USA.
FEMS Immunol Med Microbiol. 2010 Aug;59(3):493-503. doi: 10.1111/j.1574-695X.2010.00710.x. Epub 2010 Jun 7.
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.
白色念珠菌和金黄色葡萄球菌这两种真菌和细菌导致了大多数医院获得性感染,并且常常作为复杂的多微生物生物膜共同感染重症患者。为了研究多微生物生长过程中的生物膜结构,利用共聚焦扫描激光显微镜对双物种生物膜进行成像。分析揭示了一种独特的生物膜结构,其中金黄色葡萄球菌通常与白色念珠菌的菌丝成分相关联。这种物理相互作用可能为葡萄球菌提供一种侵袭策略,因为念珠菌菌丝可以穿透上皮层。为了进一步了解可能导致先前在共感染期间所证明的增强毒力的分子机制,进行了蛋白质表达研究。差异凝胶电泳鉴定出共有27种蛋白质在共培养生物膜生长期间由这些生物体显著差异产生。上调的葡萄球菌蛋白质中有L-乳酸脱氢酶1,它赋予对宿主衍生的氧化应激源的抗性。下调的蛋白质中有毒力因子的全局转录阻遏物CodY。这些发现表明,菌丝介导的金黄色葡萄球菌致病性增强可能不仅归因于物理相互作用,还可归因于多微生物生长期间诱导的特定毒力因子的差异调节。有必要在分子水平上进一步表征这些病原体之间复杂的相互作用,因为这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。