Kim Seo-Young, Kim Minjun, Kim Tae-Jong
Department of Forest Products and Biotechnology, Kookmin University, Seoul 02707, Republic of Korea.
Microorganisms. 2023 Sep 23;11(10):2376. doi: 10.3390/microorganisms11102376.
is a commensal skin bacterium and a causative agent of infectious diseases. Biofilm formation in is a mechanism that facilitates the emergence of resistant strains. This study proposes a mechanism for the regulation of biofilm formation in . through strain-specific physiological changes induced by the plant steroid diosgenin. A comparison of diosgenin-induced changes in the expression of regulatory genes associated with physiological changes revealed the intracellular regulatory mechanisms involved in biofilm formation. Diosgenin reduced biofilm formation in . ATCC 6538 and methicillin-resistant . (MRSA) CCARM 3090 by 39% and 61%, respectively. Conversely, it increased biofilm formation in . ATCC 29213 and MRSA CCARM 3820 by 186% and 582%, respectively. Cell surface hydrophobicity and extracellular protein and carbohydrate contents changed in a strain-specific manner in response to biofilm formation. An assessment of the changes in gene expression associated with biofilm formation revealed that diosgenin treatment decreased the expression of and and increased the expression of , , , and in . ATCC 6538 and MRSA CCARM 3090; however, contrasting gene expression changes were noted in . ATCC 29213 and MRSA CCARM 3820. These results suggest that a regulatory mechanism of biofilm formation is that activated expression sequentially increases the expression of , , and . This increased expression decreases the expression of , a surface-associated adhesion factor. An additional regulatory mechanism of biofilm formation is that activated expression decreases the expression of an unknown regulator that increases the expression of . This in turn decreases the expression of , which decreases the synthesis of polysaccharide intercellular adhesins and ultimately inhibits biofilm formation. By assessing strain-specific contrasting regulatory signals induced by diosgenin in . without gene mutation, this study elucidated the signal transduction mechanisms that regulate biofilm formation based on physiological and gene expression changes.
是一种皮肤共生细菌，也是传染病的病原体。在其中形成生物膜是促进耐药菌株出现的一种机制。本研究提出了一种通过植物甾体薯蓣皂苷元诱导的菌株特异性生理变化来调节生物膜形成的机制。对与生理变化相关的调控基因表达中薯蓣皂苷元诱导的变化进行比较，揭示了生物膜形成所涉及的细胞内调控机制。薯蓣皂苷元分别使金黄色葡萄球菌ATCC 6538和耐甲氧西林金黄色葡萄球菌（MRSA）CCARM 3090中的生物膜形成减少了39%和61%。相反，它分别使金黄色葡萄球菌ATCC 29213和MRSA CCARM 3820中的生物膜形成增加了186%和582%。细胞表面疏水性以及细胞外蛋白质和碳水化合物含量响应生物膜形成而以菌株特异性方式发生变化。对与生物膜形成相关的基因表达变化进行评估发现，在金黄色葡萄球菌ATCC 6538和MRSA CCARM 3090中，薯蓣皂苷元处理降低了 和 的表达，并增加了 、 、 和 的表达；然而，在金黄色葡萄球菌ATCC 29213和MRSA CCARM 3820中观察到了相反基因表达变化。这些结果表明，生物膜形成的一种调控机制是，激活的 表达依次增加 、 和 的表达。这种增加的 表达降低了表面相关粘附因子 的表达。生物膜形成的另一种调控机制是，激活的 表达降低了一种未知调节因子的表达，该调节因子增加了 的表达。这进而降低了 的表达，减少了细胞间多糖粘附素的合成并最终抑制生物膜形成。通过评估薯蓣皂苷元在无基因突变的金黄色葡萄球菌中诱导的菌株特异性对比调控信号，本研究基于生理和基因表达变化阐明了调节生物膜形成的信号转导机制。
