Abstract
The key of success of extraintestinal pathogenic Escherichia coli (ExPEC) to colonize niches outside the intestinal tract and to establish infection is the coordinated action of numerous virulence and fitness factors. The so-called high-pathogenicity island (HPI), responsible for synthesis, secretion and uptake of the siderophore yersiniabactin, proved to be an important virulence determinant. In this study we investigated the interaction of the flagellum-mediated motility and the HPI. The impairment of yersiniabactin production by deletion of irp2 or ybtA affected significantly motility. The gain of yersiniabactin production improved motility in both pathogenic and non-pathogenic E. coli strains. The loss of flagella expression had no adverse effect on the HPI. Strikingly, external iron abundance was not able to suppress activation of the HPI during motility. The HPI activity of swarming bacteria was comparable to iron deplete conditions, and could even be maximized by supplementing excessive iron. This fact is the first description of a regulatory mechanism, which does not follow the known hierarchical regulation of siderophore systems. Transcriptional reporter fusions of the ybtA promoter demonstrated that the entire promoter region with all YbtA binding sites is necessary for complete induction in both HPI-positive and HPI-negative strains. Altogether, these results suggest that the HPI is part of a complex regulatory network, which orchestrates various virulence mechanisms to optimize the overall fitness of ExPEC.
Highlights
Over the last decades the growing body of evidence was helpful to elucidate the pathogenic potential of extraintestinal pathogenic E. coli (ExPEC) [1,2,3]
In a first attempt to determine the role of the high-pathogenicity island (HPI) in flagellum-mediated motility, defined mutations affecting genes involved in the biosynthesis of yersiniabactin were generated in the prototypic uropathogenic E. coli (UPEC) strain NU14
LB is considered to be a rich medium with excess of iron available, measuring of the diameter of swimming bacteria revealed a reduction of motility compared to the wild type strain
Summary
Over the last decades the growing body of evidence was helpful to elucidate the pathogenic potential of extraintestinal pathogenic E. coli (ExPEC) [1,2,3]. The orchestrated action of a plethora of virulence and fitness factors enables ExPEC to colonize and to establish infections outside the intestinal tract resulting in diseases like urinary tract infection (UTI), neonatal meningitis, sepsis, intraabdominal infection, pneumonia, osteomyelitis, cellulitis and wound infection. Transcriptomic and proteomic approaches were performed to identify determinants essential to the pathogenesis of UTI [4,5,6]. It is striking to note that iron acquisition systems always proved to be key players.
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