Type 1 fimbrial expression enhances Escherichia coli virulence for the urinary tract
(1996) In Proceedings of the National Academy of Sciences of the United States of America 93(18). p.9827-9832- Abstract
Type 1 fimbriae are adhesion organelles expressed by many Gram-negative bacteria. They facilitate adherence to mucosal surfaces and inflammatory cells in vitro, but their contribution to virulence has not been defined. This study presents evidence that type 1 fimbriae increase the virulence of Escherichia coli for the urinary tract by promoting bacterial persistence and enhancing the inflammatory response to infection. In a clinical study, we observed that disease severity was greater in children infected with E. coli O1:K1:H7 isolates expressing type 1 fimbriae than in those infected with type 1 negative isolates of the same serotype. The E. coli O1:K1:H7 isolates had the same electrophoretic type, were hemolysin-negative, expressed P... (More)
Type 1 fimbriae are adhesion organelles expressed by many Gram-negative bacteria. They facilitate adherence to mucosal surfaces and inflammatory cells in vitro, but their contribution to virulence has not been defined. This study presents evidence that type 1 fimbriae increase the virulence of Escherichia coli for the urinary tract by promoting bacterial persistence and enhancing the inflammatory response to infection. In a clinical study, we observed that disease severity was greater in children infected with E. coli O1:K1:H7 isolates expressing type 1 fimbriae than in those infected with type 1 negative isolates of the same serotype. The E. coli O1:K1:H7 isolates had the same electrophoretic type, were hemolysin-negative, expressed P fimbriae, and carried the fim DNA sequences. When tested in a mouse urinary tract infection model, the type 1-positive E. coli O1:K1:H7 isolates survived in higher numbers, and induced a greater neutrophil influx into the urine, than O1:K1:H7 type 1-negative isolates. To confirm a role of type 1 fimbriae, a fimH null mutant (CNI016) was constructed from an O1:K1:H7 type 1-positive parent. E. coli CNI016 had reduced survival and inflammatogenicity in the mouse urinary tract infection model. E. coli CNI016 reconstituted with type 1 fimbriae (E. coli CN1018) had restored virulence similar to that of the wild- type parent strain. These results show that type 1 fimbriae in the genetic background of a uropathogenic strain contribute to the pathogenesis of E. coli in the urinary tract.
(Less)
- author
- Connell, H. LU ; Agace, W. LU ; Klemm, P. ; Schembri, M. ; Mårild, S. and Svanborg, C. LU
- organization
- publishing date
- 1996-09-03
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- adherence, inflammation, neutrophil influx, urinary tract infection
- in
- Proceedings of the National Academy of Sciences of the United States of America
- volume
- 93
- issue
- 18
- pages
- 6 pages
- publisher
- National Academy of Sciences
- external identifiers
-
- scopus:0029840463
- pmid:8790416
- ISSN
- 0027-8424
- DOI
- 10.1073/pnas.93.18.9827
- language
- English
- LU publication?
- yes
- id
- f5ec946d-94fa-462a-ab05-8670a6990886
- date added to LUP
- 2019-05-30 13:53:21
- date last changed
- 2024-04-30 11:10:57
@article{f5ec946d-94fa-462a-ab05-8670a6990886,
abstract = {{<p>Type 1 fimbriae are adhesion organelles expressed by many Gram-negative bacteria. They facilitate adherence to mucosal surfaces and inflammatory cells in vitro, but their contribution to virulence has not been defined. This study presents evidence that type 1 fimbriae increase the virulence of Escherichia coli for the urinary tract by promoting bacterial persistence and enhancing the inflammatory response to infection. In a clinical study, we observed that disease severity was greater in children infected with E. coli O1:K1:H7 isolates expressing type 1 fimbriae than in those infected with type 1 negative isolates of the same serotype. The E. coli O1:K1:H7 isolates had the same electrophoretic type, were hemolysin-negative, expressed P fimbriae, and carried the fim DNA sequences. When tested in a mouse urinary tract infection model, the type 1-positive E. coli O1:K1:H7 isolates survived in higher numbers, and induced a greater neutrophil influx into the urine, than O1:K1:H7 type 1-negative isolates. To confirm a role of type 1 fimbriae, a fimH null mutant (CNI016) was constructed from an O1:K1:H7 type 1-positive parent. E. coli CNI016 had reduced survival and inflammatogenicity in the mouse urinary tract infection model. E. coli CNI016 reconstituted with type 1 fimbriae (E. coli CN1018) had restored virulence similar to that of the wild- type parent strain. These results show that type 1 fimbriae in the genetic background of a uropathogenic strain contribute to the pathogenesis of E. coli in the urinary tract.</p>}},
author = {{Connell, H. and Agace, W. and Klemm, P. and Schembri, M. and Mårild, S. and Svanborg, C.}},
issn = {{0027-8424}},
keywords = {{adherence; inflammation; neutrophil influx; urinary tract infection}},
language = {{eng}},
month = {{09}},
number = {{18}},
pages = {{9827--9832}},
publisher = {{National Academy of Sciences}},
series = {{Proceedings of the National Academy of Sciences of the United States of America}},
title = {{Type 1 fimbrial expression enhances Escherichia coli virulence for the urinary tract}},
url = {{http://dx.doi.org/10.1073/pnas.93.18.9827}},
doi = {{10.1073/pnas.93.18.9827}},
volume = {{93}},
year = {{1996}},
}