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Infection and Immunity, November 2005, p. 7644-7656, Vol. 73, No. 11
0019-9567/05/$08.00+0 doi:10.1128/IAI.73.11.7644-7656.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
Role of Motility in the Colonization of Uropathogenic Escherichia coli in the Urinary Tract
M. Chelsea Lane,1
Virginia Lockatell,2
Greta Monterosso,3
Daniel Lamphier,2
Julia Weinert,3
J. Richard Hebel,4
David E. Johnson,2,5 and
Harry L. T. Mobley3*
Department of Microbiology and Immunology,1
Division of Infectious Diseases,2
Department of Epidemiology, University of Maryland School of Medicine,4
Research Service, Department of Veterans Affairs, Baltimore, Maryland 21201,5
Department of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, Michigan 481093
Received 16 May 2005/
Returned for modification 30 June 2005/
Accepted 26 July 2005
Uropathogenic Escherichia coli (UPEC) causes most uncomplicated urinary tract infections (UTIs) in humans. Flagellum-mediated motility and chemotaxis have been suggested to contribute to virulence by enabling UPEC to escape host immune responses and disperse to new sites within the urinary tract. To evaluate their contribution to virulence, six separate flagellar mutations were constructed in UPEC strain CFT073. The mutants constructed were shown to have four different flagellar phenotypes: fliA and fliC mutants do not produce flagella; the flgM mutant has similar levels of extracellular flagellin as the wild type but exhibits less motility than the wild type; the motAB mutant is nonmotile; and the cheW and cheY mutants are motile but nonchemotactic. Virulence was assessed by transurethral independent challenges and cochallenges of CBA mice with the wild type and each mutant. CFU/ml of urine or CFU/g bladder or kidney was determined 3 days postinoculation for the independent challenges and at 6, 16, 48, 60, and 72 h postinoculation for the cochallenges. While these mutants colonized the urinary tract during independent challenge, each of the mutants was outcompeted by the wild-type strain to various degrees at specific time points during cochallenge. Altogether, these results suggest that flagella and flagellum-mediated motility/chemotaxis may not be absolutely required for virulence but that these traits contribute to the fitness of UPEC and therefore significantly enhance the pathogenesis of UTIs caused by UPEC.
* 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. 7644-7656, Vol. 73, No. 11
0019-9567/05/$08.00+0 doi:10.1128/IAI.73.11.7644-7656.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
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