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Molecular basis of commensalism in the urinary tract: low virulence or virulence attenuation?

Zdziarski, J ; Svanborg, Catharina LU ; Wullt, Björn LU ; Hacker, J and Dobrindt, U (2008) In Infection and Immunity 76(2). p.695-703
Abstract
In some patients Escherichia coli strains establish significant bacteriuria without causing symptoms of urinary tract infection (UTI). These asymptomatic bacteriuria (ABU) strains have been shown to express fewer virulence factors than the uropathogenic E. coli (UPEC) strains that cause severe, symptomatic UTI. Paradoxically, ABU strains carry many typical UPEC virulence genes, however, and the molecular basis of their low virulence therefore remains unclear. This study examined if ABU strains may evolve from UPEC by genome loss and virulence gene attenuation. The presence of conserved E. coli K-12 genes was examined using an E. coli K-12 strain MG1655-specific DNA array and the distribution of UPEC virulence-related genes with the E. coli... (More)
In some patients Escherichia coli strains establish significant bacteriuria without causing symptoms of urinary tract infection (UTI). These asymptomatic bacteriuria (ABU) strains have been shown to express fewer virulence factors than the uropathogenic E. coli (UPEC) strains that cause severe, symptomatic UTI. Paradoxically, ABU strains carry many typical UPEC virulence genes, however, and the molecular basis of their low virulence therefore remains unclear. This study examined if ABU strains may evolve from UPEC by genome loss and virulence gene attenuation. The presence of conserved E. coli K-12 genes was examined using an E. coli K-12 strain MG1655-specific DNA array and the distribution of UPEC virulence-related genes with the E. coli pathoarray. Two groups of strains could be distinguished. Several ABU strains were shown by multi locus sequence typing and by comparative genomic analyses to be related to UPEC but to have smaller genome sizes. There were significant alterations in essential virulence genes, including reductive evolution by point mutations, DNA rearrangements and deletions. Other strains were unrelated to UPEC and lacked most of the virulence-associated genes. The results suggest that some ABU strains arise from virulent strains by attenuation of virulence genes while others are non-virulent and resemble commensal strains. We propose that virulence attenuation might constitute a general mechanism for mucosal pathogens to evolve towards commensalism. (Less)
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author
; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Infection and Immunity
volume
76
issue
2
pages
695 - 703
publisher
American Society for Microbiology
external identifiers
  • pmid:18039831
  • wos:000252978600027
  • scopus:39149129083
  • pmid:18039831
ISSN
1098-5522
DOI
10.1128/IAI.01215-07
language
English
LU publication?
yes
id
42a3482c-c0b7-4400-b15e-91f3278189cb (old id 1142646)
date added to LUP
2016-04-01 12:21:03
date last changed
2022-04-13 17:49:55
@article{42a3482c-c0b7-4400-b15e-91f3278189cb,
  abstract     = {{In some patients Escherichia coli strains establish significant bacteriuria without causing symptoms of urinary tract infection (UTI). These asymptomatic bacteriuria (ABU) strains have been shown to express fewer virulence factors than the uropathogenic E. coli (UPEC) strains that cause severe, symptomatic UTI. Paradoxically, ABU strains carry many typical UPEC virulence genes, however, and the molecular basis of their low virulence therefore remains unclear. This study examined if ABU strains may evolve from UPEC by genome loss and virulence gene attenuation. The presence of conserved E. coli K-12 genes was examined using an E. coli K-12 strain MG1655-specific DNA array and the distribution of UPEC virulence-related genes with the E. coli pathoarray. Two groups of strains could be distinguished. Several ABU strains were shown by multi locus sequence typing and by comparative genomic analyses to be related to UPEC but to have smaller genome sizes. There were significant alterations in essential virulence genes, including reductive evolution by point mutations, DNA rearrangements and deletions. Other strains were unrelated to UPEC and lacked most of the virulence-associated genes. The results suggest that some ABU strains arise from virulent strains by attenuation of virulence genes while others are non-virulent and resemble commensal strains. We propose that virulence attenuation might constitute a general mechanism for mucosal pathogens to evolve towards commensalism.}},
  author       = {{Zdziarski, J and Svanborg, Catharina and Wullt, Björn and Hacker, J and Dobrindt, U}},
  issn         = {{1098-5522}},
  language     = {{eng}},
  number       = {{2}},
  pages        = {{695--703}},
  publisher    = {{American Society for Microbiology}},
  series       = {{Infection and Immunity}},
  title        = {{Molecular basis of commensalism in the urinary tract: low virulence or virulence attenuation?}},
  url          = {{http://dx.doi.org/10.1128/IAI.01215-07}},
  doi          = {{10.1128/IAI.01215-07}},
  volume       = {{76}},
  year         = {{2008}},
}