Type 1 fimbrial expression enhances Escherichia coli virulence for the urinary tract

Connell, H., Agace, W., Schembri, M. and Marild, S. (1996) Type 1 fimbrial expression enhances Escherichia coli virulence for the urinary tract. Proceedings of the National Academy of Sciences of the United States of America, 93 18: 9827-9832. doi:10.1073/pnas.93.18.9827


Author Connell, H.
Agace, W.
Schembri, M.
Marild, S.
Title Type 1 fimbrial expression enhances Escherichia coli virulence for the urinary tract
Journal name Proceedings of the National Academy of Sciences of the United States of America   Check publisher's open access policy
ISSN 0027-8424
Publication date 1996-09-01
Sub-type Article (original research)
DOI 10.1073/pnas.93.18.9827
Open Access Status Not Open Access
Volume 93
Issue 18
Start page 9827
End page 9832
Total pages 6
Place of publication Washington, DC, United States
Publisher National Academy of Sciences
Language eng
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 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.
Keyword Urinary tract infection
Inflammation
Adherence
Neutrophil influx
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: School of Chemistry and Molecular Biosciences
 
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