Institute of Medical Microbiology and Hygiene, Saarland University, 66421 Homburg, Germany.
Institute for Medical Microbiology, Virology and Hygiene, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.
Int J Mol Sci. 2022 Mar 17;23(6):3255. doi: 10.3390/ijms23063255.
is a common cause of device related infections on which pathogens form biofilms (i.e., multilayered cell populations embedded in an extracellular matrix). Here, we report that the transcription factor SpoVG is essential for the capacity of to form such biofilms on artificial surfaces under in vitro conditions. Inactivation of in the polysaccharide intercellular adhesin (PIA) producing strain 1457 yielded a mutant that, unlike its parental strain, failed to produce a clear biofilm in a microtiter plate-based static biofilm assay. A decreased biofilm formation capacity was also observed when 1457 Δ cells were co-cultured with polyurethane-based peripheral venous catheter fragments under dynamic conditions, while the -complemented 1457 Δ derivative formed biofilms comparable to the levels seen with the wild-type. Transcriptional studies demonstrated that the deletion of significantly altered the expression of the intercellular adhesion () locus by upregulating the transcription of the operon repressor and down-regulating the transcription of . Electrophoretic mobility shift assays (EMSA) revealed an interaction between SpoVG and the - intergenic region, suggesting SpoVG to promote biofilm formation of by modulating expression. However, when mice were challenged with the 1457 Δ mutant in a foreign body infection model, only marginal differences in biomasses produced on the infected catheter fragments between the mutant and the parental strain were observed. These findings suggest that SpoVG is critical for the PIA-dependent biofilm formation of under in vitro conditions, but is largely dispensable for biofilm formation of this skin commensal under in vivo conditions.
是一种常见的器械相关感染病原体,其病原体形成生物膜(即嵌入细胞外基质中的多层细胞群体)。在这里,我们报告转录因子 SpoVG 对于在体外条件下在人工表面上形成生物膜的能力是必不可少的。在多糖细胞间黏附素(PIA)产生 菌株 1457 中失活 导致突变体,与亲本菌株不同,其在微量滴定板静态生物膜测定中无法产生清晰的生物膜。当 1457 Δ细胞与基于聚氨酯的外周静脉导管片段在动态条件下共培养时,也观察到生物膜形成能力降低,而 互补 1457 Δ衍生物形成的生物膜与野生型相当。转录研究表明, 的缺失通过上调 操纵子抑制剂 和下调 的转录,显著改变了细胞间黏附( )基因座的表达。电泳迁移率变动分析(EMSA)显示 SpoVG 与 基因间区之间存在相互作用,表明 SpoVG 通过调节 表达促进 生物膜的形成。然而,当小鼠在异物感染模型中受到 1457 Δ突变体的挑战时,在感染的导管片段上观察到突变体和亲本菌株之间产生的生物量仅存在微小差异。这些发现表明,SpoVG 对于在体外条件下 PIA 依赖性生物膜形成至关重要,但在体内条件下对于这种皮肤共生菌的生物膜形成在很大程度上是可有可无的。