In Vivo Dynamics of Type 1 Fimbria Regulation in Uropathogenic
            <i>Escherichia coli</i>
            during Experimental Urinary Tract Infection

Gunther, Nereus W.; Lockatell, Virginia; Johnson, David E.; Mobley, Harry L. T.

doi:10.1128/iai.69.5.2838-2846.2001

Cited by 102 publications

(88 citation statements)

References 42 publications

(41 reference statements)

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“…In another study, we observed differing temporal regulation of the type 1 fimbrial invertible element between strains in vivo during murine UTI (12). Cystitis isolates were mostly phase on throughout infection, and pyelonephritis isolates tended to be phase on only early during infection (24 h postinfection) and primarily phase off thereafter.…”

Section: Discussionmentioning

confidence: 86%

Coordinate Expression of Fimbriae in Uropathogenic Escherichia coli

Snyder¹,

et al. 2005

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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.Uropathogenic Escherichia coli (UPEC) strains cause the majority of all urinary tract infections (UTIs). Forty to 50% of women experience at least one UTI during their lifetime, leading to an estimated 8 million physician visits annually in the United States (39, 55). Recent efforts to understand the mechanisms of virulence in this important pathogen include the sequencing of UPEC (52), complete transcriptome analysis (45), signature-tagged mutagenesis (4), and differential fluorescence induction (33). These studies collectively implicate adhesins, iron acquisition systems, capsules, lipopolysaccharides, and toxins in UPEC pathogenesis.Adherence to host tissues is often the first step towards colonization; thus, adhesins are essential for pathogenesis. The recent sequencing of UPEC strain CFT073, along with previous virulence studies, has predicted or demonstrated as many as 12 fimbrial gene clusters in this strain (5, 17, 52). Many fimbrial and afimbrial adhesins are phase variable (28, 34), including the most ubiquitous type 1 fimbriae encoded by the fim gene cluster. The expression of type 1 fimbriae is controlled by a promoter situated on an invertible element of DNA, also referred to as the fim switch (1). Bacteria are phase on, and type 1 fimbriae are expressed when the promoter faces the direction of fimA, which encodes the main structur...

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Section: Discussionmentioning

confidence: 86%

Coordinate Expression of Fimbriae in Uropathogenic Escherichia coli

Snyder¹,

et al. 2005

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“…In vivo expression of type 1 fimbriae contributes to virulence in the urinary tract and fim expression is critical for infection of the lower urinary tract (cystitis) (Bahrani-Mougeot et al, 2002;Gunther et al, 2001).…”

Section: Biofilm Formationmentioning

confidence: 99%

Regulation of type 1 fimbriae synthesis and biofilm formation by the transcriptional regulator LrhA of Escherichia coli

et al. 2005

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Type 1 fimbriae of Escherichia coli facilitate attachment to the host mucosa and promote biofilm formation on abiotic surfaces. The transcriptional regulator LrhA, which is known as a repressor of flagellar, motility and chemotaxis genes, regulates biofilm formation and expression of type 1 fimbriae. Whole-genome expression profiling revealed that inactivation of lrhA results in an increased expression of structural components of type 1 fimbriae. In vitro, LrhA bound to the promoter regions of the two fim recombinases (FimB and FimE) that catalyse the inversion of the fimA promoter, and to the invertible element itself. Translational lacZ fusions with these genes and quantification of fimE transcript levels by real-time PCR showed that LrhA influences type 1 fimbrial phase variation, primarily via activation of FimE, which is required for the ON-to-OFF transition of the fim switch. Enhanced type 1 fimbrial expression as a result of lrhA disruption was confirmed by mannose-sensitive agglutination of yeast cells. Biofilm formation was stimulated by lrhA inactivation and completely suppressed upon LrhA overproduction. The effects of LrhA on biofilm formation were exerted via the changed levels of surface molecules, most probably both flagella and type 1 fimbriae. Together, the data show a role for LrhA as a repressor of type 1 fimbrial expression, and thus as a regulator of the initial stages of biofilm development and, presumably, bacterial adherence to epithelial host cells also.

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Section: Introductionmentioning

confidence: 99%

“…This may be important to further limit immune exposure and also to prevent the physical interference of one adhesin with another. Moreover, such cross-talk may be important to define the progression of an infection (Gunther et al, 2001;Holden & Gally, 2004).The aim of this study was to determine whether cross-talk between P and type 1 fimbriae occurs in E. coli clinical isolates with the levels of PapB that are produced from its natural promoter on the chromosome. Fifty clinical E. coli isolates associated with pyelonephritis, cystitis or asymptomatic carriage were used for the study.…”

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confidence: 99%

Demonstration of regulatory cross-talk between P fimbriae and type 1 fimbriae in uropathogenic Escherichia coli

et al. 2006

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The majority of Escherichia coli strains isolated from urinary tract infections have the potential to express multiple fimbriae. Two of the most common fimbrial adhesins are type 1 fimbriae and pyelonephritis-associated pili (Pap). Previous research has shown that induced, plasmid-based expression of a Pap regulator, papB, and its close homologues can prevent inversion of the fim switch controlling the expression of type 1 fimbriae. The aim of the present study was to determine if this cross-regulation occurs when PapB is expressed from its native promoter in the chromosome of E. coli K-12 and clinical isolates. The regulation was examined in three ways: (1) mutated alleles of the pap regulatory region, including papB and papI, that maintain the pap promoter in either the off or the on phase were exchanged into the chromosome of both E. coli K-12 and the clinical isolate E. coli CFT073, and the effect on type 1 fimbrial expression was measured; (2) type 1 fimbrial expression was determined using a novel fimS : : gfp + reporter system in mutants of the clinical isolate E. coli 536 in which combinations of complete fimbrial clusters had been deleted; (3) type 1 fimbrial expression was determined in a range of clinical isolates and compared with both the number of P clusters and their expression. All three approaches demonstrated that P expression represses type 1 fimbrial expression. Using a number of novel genetic approaches, this work extends the initial finding that PapB inhibits FimB recombination to the impact of this regulation in clinical isolates. INTRODUCTIONUrinary tract infections (UTIs) are common, affecting a large proportion of the population. It is estimated that 20 % of women develop a UTI in their lifetime, and antibiotic treatment results in approximately 110 000 prescriptions per million inhabitants per annum in Europe (Naber, 2000). Escherichia coli strains are the predominant cause of uncomplicated UTIs, responsible for between 60 and 80 % of the cases reported in the UK each year (Graham & Galloway, 2001). Many infections are asymptomatic, especially in the elderly (Nicolle, 2001), but others result in cystitis. If the infection ascends to the kidney, then pyelonephritis can occur. Such infections are a significant origin of Gramnegative sepsis.Fimbrial adhesins are important virulence factors that allow binding of the bacteria to specific receptors on epithelial cells of the urinary tract. The two adhesins most commonly associated with UTI are type 1 fimbriae, and pyelonephritisassociated pili (Pap) and Pap-related fimbriae (Prf); the last two are collectively termed P fimbriae in this study. Type 1 fimbriae mediate binding to a-D-mannose-containing receptors and extracellular matrix components, whereas P fimbriae bind to glycoreceptors containing the aGal(1-4)bGal moiety (Lindberg et al., 1984). Although type 1 fimbriae are common to the majority of E. coli isolates, the FimH adhesin has been shown to be important in a mouse model of UTI, and a degranulation response to the fimbriae is asso...

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In Vivo Dynamics of Type 1 Fimbria Regulation in Uropathogenic Escherichia coli during Experimental Urinary Tract Infection

Cited by 102 publications

References 42 publications

Coordinate Expression of Fimbriae in Uropathogenic Escherichia coli

Coordinate Expression of Fimbriae in Uropathogenic Escherichia coli

Regulation of type 1 fimbriae synthesis and biofilm formation by the transcriptional regulator LrhA of Escherichia coli

Demonstration of regulatory cross-talk between P fimbriae and type 1 fimbriae in uropathogenic Escherichia coli

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