Affiliation:
1. Institute of Medical Microbiology and Immunology, University of Pécs, 7624 Pécs, Hungary
2. Institut für Molekulare Infektionsbiologie, Universität Würzburg, 97070 Würzburg, Germany
Abstract
ABSTRACT
RfaH is a regulatory protein in
Escherichia coli
and
Salmonella enterica
serovar Typhimurium. Although it enhances expression of different factors that are proposed to play a role in bacterial virulence, a direct effect of RfaH on virulence has not been investigated so far. We report that inactivation of
rfaH
dramatically decreases the virulence of uropathogenic
E. coli
strain 536 in an ascending mouse model of urinary tract infection. The mortality rate caused by the wild-type strain in this assay is 100%, whereas that of its isogenic
rfaH
mutant does not exceed 18%. In the case of coinfection, the wild-type strain 536 shows higher potential to colonize the urinary tract even when it is outnumbered 100-fold by its
rfaH
mutant in the inoculum. In contrast to the wild-type strain, serum resistance of strain 536
rfaH
::
cat
is fully abolished. Furthermore, we give evidence that, besides a major decrease in the amount of hemin receptor ChuA (G. Nagy, U. Dobrindt, M. Kupfer, L. Emody, H. Karch, and J. Hacker, Infect. Immun. 69:1924-1928, 2001), loss of the RfaH protein results in an altered lipopolysaccharide phenotype as well as decreased expression of K15 capsule and alpha-hemolysin, whereas levels of other pathogenicity factors such as siderophores, flagella, Prf, and S fimbriae appear to be unaltered in strain 536
rfaH
::
cat
in comparison to the wild-type strain.
trans c
omplementation of the mutant strain with the
rfaH
gene restores wild-type levels of the affected virulence factors and consequently restitutes virulence in the mouse model of ascending urinary tract infection.
Publisher
American Society for Microbiology
Subject
Infectious Diseases,Immunology,Microbiology,Parasitology
Cited by
85 articles.
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