PapG-dependent adherence breaks mucosal inertia and triggers the innate host response
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/277902
- author
- Bergsten, Göran LU ; Samuelsson, Martin LU ; Wullt, Björn LU ; Leijonhufvud, Irene LU ; Fischer, Hans LU and Svanborg, Catharina LU
- organization
- publishing date
- 2004
- 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
- 2016-04-01 16:10:13
- date last changed
- 2022-01-28 17:49:56
@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}}, doi = {{10.1086/383278}}, volume = {{189}}, year = {{2004}}, }