Abstract
The effect of a urinary tract infection on the host is a well-studied research field. However, how the host immune response affects uropathogenic Escherichia coli (CFT073) virulence is less studied. The aim of the present study was to investigate the impact of proinflammatory cytokine exposure on the virulence of uropathogenic Escherichia coli. We found that all tested proinflammatory cytokines (TNF-α, IL-1β, IL-6, IL-8 and IFN-γ) induced an increased CFT073 growth. We also found that biofilm formation and hemolytic activity was reduced in the presence of all proinflammatory cytokines. However, a reduction in siderophore release was only observed in the presence of IL-1β, IL-6 and IL-8. Real time-qPCR showed that all proinflammatory cytokines except TNF-α significantly increased genes associated with the iron acquisition system in CFT073. We also found that the proinflammatory cytokines induced significant changes in type-1 fimbriae, P-fimbriae and gluconeogenetic genes. Furthermore, we also showed, using a Caenorhabditis elegans (C. elegans) killing assay that all cytokines decreased the survival of C. elegans worms significantly. Taken together, our findings show that proinflammatory cytokines have the ability to alter the virulence traits of UPEC.
Highlights
Escherichia coli (E. coli) is a ubiquitous member of the intestinal microbiota and it is by far the most common etiological agent in urinary tract infection (UTI)
IL-1β and above all IL-6, IL-8 and IFN-γ increased the growth of CFT073 in a concentration dependent manner in the range 4 to 8 h of stimulation compared to the unstimulated controls (Figures 1A–C)
In this study we focused on investigating the cross kingdom effects of proinflammatory cytokines on the virulence of uropathogenic E. coli (UPEC)
Summary
Escherichia coli (E. coli) is a ubiquitous member of the intestinal microbiota and it is by far the most common etiological agent in urinary tract infection (UTI). Cystitis is the phase of the infection when bacteria have ascended the urethra and infected the bladder (Flores-Mireles et al, 2015). The gene fimH codes for the adhesin part of the type-1 fimbriae that mediates binding to mannose motifs prevalent in the urinary tract on the urothelium. The fimH protein mediates UPEC invasion of the bladder epithelial cells through α3β1 integrin interactions. UPEC can ascend further up the urinary tract and infect the kidneys. P-fimbriae enable adhesion to renal epithelium through attachment to globosides, a type of glycolipid present on cells in the tubuli and collecting ducts (Korhonen et al, 1986; Flores-Mireles et al, 2015).
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