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Infection and Immunity, November 2005, p. 7588-7596, Vol. 73, No. 11
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.11.7588-7596.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Coordinate Expression of Fimbriae in Uropathogenic Escherichia coli

Jennifer A. Snyder,1 Brian J. Haugen,2 C. Virginia Lockatell,3 Nathalie Maroncle,4 Erin C. Hagan,4 David E. Johnson,3,5 Rodney A. Welch,2 and Harry L. T. Mobley4*

Department of Microbiology and Immunology,1 Division of Infectious Diseases,3 University of Maryland School of Medicine, and Department of Veterans Affairs, Baltimore, Maryland 21201,5 Department of Medical Microbiology and Immunology, University of Wisconsin—Madison, Madison, Wisconsin 53706,2 Department of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, Michigan 481094

Received 1 July 2005/ Returned for modification 22 July 2005/ Accepted 28 July 2005

Uropathogenic Escherichia coli is the most common etiological agent of urinary tract infections. Bacteria can often express multiple adhesins during infection in order to favor attachment to specific niches within the urinary tract. We have recently demonstrated that type 1 fimbria, a phase-variable virulence factor involved in adherence, was the most highly expressed adhesin during urinary tract infection. Here, we examine whether the expression of type 1 fimbriae can affect the expression of other adhesins. Type 1 fimbrial phase-locked mutants of E. coli strain CFT073, which harbors genes for numerous adhesins, were employed in this study. CFT073-specific DNA microarray analysis of these strains demonstrates that the expression of type 1 fimbriae coordinately affects the expression of P fimbriae in an inverse manner. This represents evidence for direct communication between genes relating to pathogenesis, perhaps to aid the sequential occupation of different urinary tract tissues. While the role of type 1 fimbriae during infection has been clear, the role of P fimbriae must be further defined to assert the relevance of coordinated regulation in vivo. Therefore, we examined the ability of P fimbrial isogenic mutants, constructed in a type 1 fimbrial-negative background, to compete in the murine urinary tract over a period of 168 h. No differences in the colonization of these mutants were observed. However, comparison of these results with previous studies suggests that inversely coordinated expression of adhesin gene clusters does occur in vivo. Interestingly, the mutant that was incapable of expressing either type 1 or P fimbriae compensated by synthesizing F1C fimbriae.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, University of Michigan Medical School, 5641 Medical Science Building II, 1150 West Medical Center Drive, Ann Arbor, MI 48109. Phone: (734) 763-3531. Fax: (734) 764-3562. E-mail: hmobley{at}umich.edu.

Editor: D. L. Burns

Infection and Immunity, November 2005, p. 7588-7596, Vol. 73, No. 11
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.11.7588-7596.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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