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P-fimbriae trigger mucosal responses to Escherichia coli in the human urinary tract

Wullt, Björn LU ; Bergsten, Göran LU ; Connell, Hugh LU ; Röllano, Piotr ; Gebratsedik, Negash ; Hang, Long LU and Svanborg, Catharina LU (2001) In Cellular Microbiology 3(4). p.255-264
Abstract

Uropathogenic Escherichia coli elicit a host response that determines the severity of urinary tract infection (UTI). Specific adherence mechanisms allow the bacteria to initiate this process by targeting epithelial cells in the urinary tract mucosa. Epidemiological studies show a strong association of P-fimbriae with disease severity, suggesting that adherence mediated by these organelles has a direct effect on mucosal inflammation in vivo. The present study examined the ability of P-fimbriae to induce inflammation in the human urinary tract. Patients were subjected to intravesical inoculation with a non-fimbriated E. coli strain or transformants of this strain expressing P-fimbriae. The inflammatory response was analysed as a function... (More)

Uropathogenic Escherichia coli elicit a host response that determines the severity of urinary tract infection (UTI). Specific adherence mechanisms allow the bacteria to initiate this process by targeting epithelial cells in the urinary tract mucosa. Epidemiological studies show a strong association of P-fimbriae with disease severity, suggesting that adherence mediated by these organelles has a direct effect on mucosal inflammation in vivo. The present study examined the ability of P-fimbriae to induce inflammation in the human urinary tract. Patients were subjected to intravesical inoculation with a non-fimbriated E. coli strain or transformants of this strain expressing P-fimbriae. The inflammatory response was analysed as a function of P-fimbrial expression. The P-fimbriated transformants invariably caused higher interleukin (IL)-8, IL-6 and neutrophil responses in the urinary tract than the ABU strain. Furthermore, loss of P-fimbrial expression in vivo was accompanied by a return to background levels of neutrophils, IL-6 and IL-8 in individual patients. The results demonstrate that the pap sequences confer on a non-fimbriated, avirulent strain the ability to induce a host response in the human urinary tract. P-fimbriae thus fulfil the 'molecular Koch-Henle postulates' linking a single virulence factor to host response induction.

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author
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organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Cellular Microbiology
volume
3
issue
4
pages
10 pages
publisher
Wiley-Blackwell
external identifiers
  • pmid:11298649
  • scopus:0035048239
ISSN
1462-5814
DOI
10.1046/j.1462-5822.2001.00111.x
language
English
LU publication?
yes
id
07cbb9b4-8f52-4977-83d1-7d20162a1df4
date added to LUP
2019-06-19 14:08:18
date last changed
2023-01-08 01:26:04
@article{07cbb9b4-8f52-4977-83d1-7d20162a1df4,
  abstract     = {{<p>Uropathogenic Escherichia coli elicit a host response that determines the severity of urinary tract infection (UTI). Specific adherence mechanisms allow the bacteria to initiate this process by targeting epithelial cells in the urinary tract mucosa. Epidemiological studies show a strong association of P-fimbriae with disease severity, suggesting that adherence mediated by these organelles has a direct effect on mucosal inflammation in vivo. The present study examined the ability of P-fimbriae to induce inflammation in the human urinary tract. Patients were subjected to intravesical inoculation with a non-fimbriated E. coli strain or transformants of this strain expressing P-fimbriae. The inflammatory response was analysed as a function of P-fimbrial expression. The P-fimbriated transformants invariably caused higher interleukin (IL)-8, IL-6 and neutrophil responses in the urinary tract than the ABU strain. Furthermore, loss of P-fimbrial expression in vivo was accompanied by a return to background levels of neutrophils, IL-6 and IL-8 in individual patients. The results demonstrate that the pap sequences confer on a non-fimbriated, avirulent strain the ability to induce a host response in the human urinary tract. P-fimbriae thus fulfil the 'molecular Koch-Henle postulates' linking a single virulence factor to host response induction.</p>}},
  author       = {{Wullt, Björn and Bergsten, Göran and Connell, Hugh and Röllano, Piotr and Gebratsedik, Negash and Hang, Long and Svanborg, Catharina}},
  issn         = {{1462-5814}},
  language     = {{eng}},
  month        = {{04}},
  number       = {{4}},
  pages        = {{255--264}},
  publisher    = {{Wiley-Blackwell}},
  series       = {{Cellular Microbiology}},
  title        = {{P-fimbriae trigger mucosal responses to Escherichia coli in the human urinary tract}},
  url          = {{http://dx.doi.org/10.1046/j.1462-5822.2001.00111.x}},
  doi          = {{10.1046/j.1462-5822.2001.00111.x}},
  volume       = {{3}},
  year         = {{2001}},
}