Parker Robert E, Knupp David, Al Safadi Rim, Rosenau Agnѐs, Manning Shannon D
Department of Microbiology and Molecular Genetics, Michigan State University, East Lansing, MI 48824, USA.
Infectiologie et Santé Publique ISP, Institut National de la Recherche Agronomique, Université de Tours, Equipe Bactéries et Risque Materno-fœtal, UMR1282 Tours, France.
Genes (Basel). 2017 Jan 6;8(1):23. doi: 10.3390/genes8010023.
(group B ; GBS) is a common inhabitant of the genitourinary and/or gastrointestinal tract in up to 40% of healthy adults; however, this opportunistic pathogen is able to breach restrictive host barriers to cause disease and persist in harsh and changing conditions. This study sought to identify a role for quorum sensing, a form of cell to cell communication, in the regulation of the fibrinogen-binding () two-component system and the ability to associate with decidualized endometrial cells in vitro. To do this, we created a deletion in , which encodes the putative autoinducing peptide, in a GBS strain belonging to multilocus sequence type (ST)-17 and made comparisons to the wild type. Sequence variation in the operon was detected in 40 clinical strains and a non-synonymous single nucleotide polymorphism was detected in in all of the ST-17 genomes that resulted in a truncation. Using qPCR, expression of operon genes was significantly decreased in the ST-17 mutant during exponential growth with the biggest difference (3.3-fold) occurring at higher cell densities. Association with decidualized endometrial cells was decreased 1.3-fold in the mutant relative to the wild type and expression was reduced 22-fold in following exposure to the endometrial cells. Collectively, these data suggest that this putative quorum sensing molecule is important for attachment to human tissues and demonstrate a role for RgfD in GBS pathogenesis through regulation of .
B组链球菌(GBS)是高达40%健康成年人泌尿生殖道和/或胃肠道的常见定植菌;然而,这种机会致病菌能够突破限制性宿主屏障引发疾病,并在恶劣多变的环境中持续存在。本研究旨在确定群体感应(一种细胞间通讯形式)在调节纤维蛋白原结合双组分系统以及体外与蜕膜化子宫内膜细胞结合能力方面的作用。为此,我们在一株属于多位点序列类型(ST)-17的GBS菌株中,对编码假定自诱导肽的基因进行缺失,并与野生型进行比较。在40株临床菌株中检测到操纵子的序列变异,在所有导致截断的ST-17基因组中均检测到基因的一个非同义单核苷酸多态性。使用qPCR,在指数生长期间,ST-17突变体中操纵子基因的表达显著降低,在较高细胞密度时差异最大(3.3倍)。相对于野生型,突变体与蜕膜化子宫内膜细胞的结合减少了1.3倍,在暴露于子宫内膜细胞后,基因的表达降低了22倍。总体而言,这些数据表明这种假定的群体感应分子对附着于人体组织很重要,并通过调节证明了RgfD在GBS致病机制中的作用。