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PapG-dependent adherence breaks mucosal inertia and triggers the innate host response

Bergsten, Göran LU ; Samuelsson, Martin LU ; Wullt, Björn LU ; Leijonhufvud, Irene LU ; Fischer, Hans LU and Svanborg, Catharina LU (2004) In Journal of Infectious Diseases 189(9). p.1734-1742
Abstract
Mucosal pathogens differ from normal flora constituents in that they provoke a host response that upsets mucosal integrity. We investigated whether the elaboration of discrete adherence factors is sufficient to break the inertia of the mucosal barrier. PapG-mediated adherence was selected as an example, because P fimbrial expression characterizes uropathogenic Escherichia coli and because adherence starts the attack on the mucosal barrier. Patients were inoculated intravesically with transformed nonvirulent E. coli strains expressing functional P fimbriae (E. coli pap(+)) or mutant fimbriae lacking the adhesin (E. coli DeltapapG). E. coli pap(+) was shown to activate the innate host response, and adherent gfp(+) bacteria were observed on... (More)
Mucosal pathogens differ from normal flora constituents in that they provoke a host response that upsets mucosal integrity. We investigated whether the elaboration of discrete adherence factors is sufficient to break the inertia of the mucosal barrier. PapG-mediated adherence was selected as an example, because P fimbrial expression characterizes uropathogenic Escherichia coli and because adherence starts the attack on the mucosal barrier. Patients were inoculated intravesically with transformed nonvirulent E. coli strains expressing functional P fimbriae (E. coli pap(+)) or mutant fimbriae lacking the adhesin (E. coli DeltapapG). E. coli pap(+) was shown to activate the innate host response, and adherent gfp(+) bacteria were observed on excreted uroepithelial cells. E. coli DeltapapG failed to trigger a response and was nonadhesive. We conclude that PapG-mediated adherence breaks mucosal inertia in the human urinary tract by triggering innate immunity and propose that this activation step differentiates asymptomatic carriage from infection. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Journal of Infectious Diseases
volume
189
issue
9
pages
1734 - 1742
publisher
Oxford University Press
external identifiers
  • pmid:15116313
  • wos:000220951300025
  • scopus:2442519109
ISSN
1537-6613
DOI
10.1086/383278
language
English
LU publication?
yes
id
cb838ca7-cdd7-49ae-9989-7084c0998598 (old id 277902)
date added to LUP
2007-10-17 08:37:43
date last changed
2017-09-03 04:33:52
@article{cb838ca7-cdd7-49ae-9989-7084c0998598,
  abstract     = {Mucosal pathogens differ from normal flora constituents in that they provoke a host response that upsets mucosal integrity. We investigated whether the elaboration of discrete adherence factors is sufficient to break the inertia of the mucosal barrier. PapG-mediated adherence was selected as an example, because P fimbrial expression characterizes uropathogenic Escherichia coli and because adherence starts the attack on the mucosal barrier. Patients were inoculated intravesically with transformed nonvirulent E. coli strains expressing functional P fimbriae (E. coli pap(+)) or mutant fimbriae lacking the adhesin (E. coli DeltapapG). E. coli pap(+) was shown to activate the innate host response, and adherent gfp(+) bacteria were observed on excreted uroepithelial cells. E. coli DeltapapG failed to trigger a response and was nonadhesive. We conclude that PapG-mediated adherence breaks mucosal inertia in the human urinary tract by triggering innate immunity and propose that this activation step differentiates asymptomatic carriage from infection.},
  author       = {Bergsten, Göran and Samuelsson, Martin and Wullt, Björn and Leijonhufvud, Irene and Fischer, Hans and Svanborg, Catharina},
  issn         = {1537-6613},
  language     = {eng},
  number       = {9},
  pages        = {1734--1742},
  publisher    = {Oxford University Press},
  series       = {Journal of Infectious Diseases},
  title        = {PapG-dependent adherence breaks mucosal inertia and triggers the innate host response},
  url          = {http://dx.doi.org/10.1086/383278},
  volume       = {189},
  year         = {2004},
}