Previous Article | Next Article ![]()
Infection and Immunity, July 2006, p. 4039-4047, Vol. 74, No. 7
0019-9567/06/$08.00+0 doi:10.1128/IAI.02058-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
Division of Pediatric Infectious Diseases, Johns Hopkins University School of Medicine, 600 North Wolfe St., Park 256, Baltimore, Maryland 21287,1 Division of Clinical Research, National Health Research Institutes, Tainan, Taiwan,2 Institute of Molecular Medicine, National Cheng Kung University Medical College, Tainan, Taiwan3
Received 21 December 2005/ Returned for modification 30 March 2006/ Accepted 24 April 2006
Type 1 fimbriae have been suggested to play a role in the pathogenesis of extraintestinal Escherichia coli infection. Type 1 fimbriation in E. coli is phase variable and known to be dependent upon FimB and FimE, the two recombinases that invert the molecular switch fimS and control the expression of the downstream fim operon. Here we showed that HbiF, a novel site-specific recombinase, inverted fimS independently of FimB and FimE. HbiF-mediated fimS inversion appeared to be predominantly switching from "off" (termed OFF) to "on" (termed ON) orientation. This is different from the fimS inversion mediated by either FimB (bidirectional ON to OFF and OFF to ON) or FimE (unidirectional ON to OFF). Constitutive expression of the hbiF gene in E. coli resulted in a fimS-locked-ON phenotype, which resulted in the pathogenic E. coli K1 strain being incapable of inducing a high degree of bacteremia in neonatal rats. Discovery of HbiF-mediated OFF-to-ON fimS switching provides a new opportunity to develop a strategy for the prevention and therapy of extraintestinal E. coli infection including bacteremia and meningitis.
This article has been cited by other articles:
| J. Bacteriol. | J. Virol. | Eukaryot. Cell |
|---|
| Microbiol. Mol. Biol. Rev. | Clin. Vaccine Immunol. | All ASM Journals |
|---|