Abstract
Uropathogenic Escherichia coli (UPEC) is the major causative agent of uncomplicated urinary tract infections (UTIs). A common virulence genotype of UPEC strains responsible for UTIs is yet to be defined, due to the large variation of virulence factors observed in UPEC strains. We hypothesized that studying UPEC functional responses in patients might reveal universal UPEC features that enable pathogenesis. Here we identify a transcriptional program shared by genetically diverse UPEC strains isolated from 14 patients during uncomplicated UTIs. Strikingly, this in vivo gene expression program is marked by upregulation of translational machinery, providing a mechanism for the rapid growth within the host. Our analysis indicates that switching to a more specialized catabolism and scavenging lifestyle in the host allows for the increased translational output. Our study identifies a common transcriptional program underlying UTIs and illuminates the molecular underpinnings that likely facilitate the fast growth rate of UPEC in infected patients.
Highlights
Urinary tract infections (UTIs) are among the most common bacterial infections in humans, affecting 150 million people each year worldwide [1]
To better understand Uropathogenic Escherichia coli (UPEC) functional responses to the human host, we isolated and sequenced RNA from the urine from fourteen otherwise healthy women diagnosed with UPEC-associated urinary tract infection
While we know that these virulence strategies are essential for establishing infection, UPEC strains can differ dramatically in the specific factors that are utilized
Summary
Urinary tract infections (UTIs) are among the most common bacterial infections in humans, affecting 150 million people each year worldwide [1]. The majority of our insights into UPEC pathogenesis have been obtained through in vitro assays, cell culture systems, and animal models [6,7,8,9]. While these studies have identified virulence and fitness factors that are important for UPEC infection, how these studies translate to human infection is not clear. The genetic heterogeneity of UPEC isolates, which carry diverse and functionally redundant virulence systems including iron acquisition, adherence, and toxins, further complicates our understanding of uropathogenesis [10,11,12,13,14]. The different constellations of virulence factors and diverse genetic backgrounds raise the question of whether different UPEC strains vary in their strategies for pathogenesis
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