Receptor Structure for F1C Fimbriae of Uropathogenic
            <i>Escherichia coli</i>

Khan, Abdul Salam; Kniep, Bernhard; Oelschlaeger, Tobias A.; Die, Irma van; Korhonen, Timo; Hacker, Jörg

doi:10.1128/iai.68.6.3541-3547.2000

Cited by 105 publications

(74 citation statements)

References 54 publications

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“…Type 1 fimbriae bind to mannose-containing receptors, and the P group fimbriae bind to the Gal␣(1-4)Gal moiety of the P blood group and related receptors, which are widely distributed on the uroepithelium (31). The high-affinity binding of F1C fimbriae to the GalNAc␤1-4Gal␤ sequence of glycolipids, asialo-GM 1 (GgO 4 Cer) and asialo-GM 2 (GgO 3 Cer), and low-affinity binding to carbohydrate structures GlcNAc␤1-3Gal␤, Gal␤1-4Glc, Gal, and Glc of glycolipids have been demonstrated recently (15).…”

Section: Discussionmentioning

confidence: 97%

Role of Enterococcus faecalis Surface Protein Esp in the Pathogenesis of Ascending Urinary Tract Infection

Shankar¹,

Lockatell

Baghdayan³

et al. 2001

Infect Immun

308

226

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Enterococcus faecalis bacteria isolated from patients with bacteremia, endocarditis, and urinary tract infections more frequently express the surface protein Esp than do fecal isolates. To assess the role of Esp in colonization and persistence of E. faecalis in an animal model of ascending urinary tract infection, we compared an Esp ؉ strain of E. faecalis to its isogenic Esp-deficient mutant. Groups of CBA/J mice were challenged transurethrally with 10 8 CFU of either the parent or mutant strain, and bacteria in the urine, bladder, and kidneys were enumerated 5 days postinfection. Significantly higher numbers of bacteria were recovered from the bladder and urine of mice challenged with the parent strain than from the bladder and urine of mice challenged with the mutant. Colonization of the kidney, however, was not significantly different between the parent and mutant strains. Histopathological evaluations of kidney and bladder tissue done at 5 days postinfection did not show marked histopathological changes consistent with inflammation, mucosal hyperplasia, or apoptosis, and there was no observable difference between the mice challenged with the parent and those challenged with the mutant. We conclude that, while Esp does not influence histopathological changes associated with acute urinary tract infections, it contributes to colonization and persistence of E. faecalis at this site.

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Section: Discussionmentioning

confidence: 97%

Role of Enterococcus faecalis Surface Protein Esp in the Pathogenesis of Ascending Urinary Tract Infection

Shankar¹,

Lockatell

Baghdayan³

et al. 2001

Infect Immun

308

226

View full text Add to dashboard Cite

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“…The presence of S fimbriae and type 1C fimbriae (172,178,340). Uropathogenic P. mirabilis isolates also contain a member of the ␥ 1 -fimbrial clade, the ambient-temperature fimbria (atf) operon; however, the encoded adhesin is not required for cystitis in a mouse model (213,214,373).…”

Section: The ␥-Fimbriaementioning

confidence: 99%

Evolution of the Chaperone/Usher Assembly Pathway: Fimbrial Classification Goes Greek

Nuccio

Bäumler

2007

Microbiol Mol Biol Rev

293

456

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SUMMARY Many Proteobacteria use the chaperone/usher pathway to assemble proteinaceous filaments on the bacterial surface. These filaments can curl into fimbrial or nonfimbrial surface structures (e.g., a capsule or spore coat). This article reviews the phylogeny of operons belonging to the chaperone/usher assembly class to explore the utility of establishing a scheme for subdividing them into clades of phylogenetically related gene clusters. Based on usher amino acid sequence comparisons, our analysis shows that the chaperone/usher assembly class is subdivided into six major phylogenetic clades, which we have termed α-, β-, γ-, κ-, π-, and σ-fimbriae. Members of each clade share related operon structures and encode fimbrial subunits with similar protein domains. The proposed classification system offers a simple and convenient method for assigning newly discovered chaperone/usher systems to one of the six major phylogenetic groups.

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“…F1C fimbriae are expressed by a large proportion of UTI E. coli strains; depending on the study, 14 to 30% of UTI strains have been reported to be able to express these fimbriae (47,60). F1C fimbriae specifically recognize galactosylceramide targets present on epithelial cells in the kidneys, ureters, and bladder, as well as globotriaosylceramide, present only in the kidneys (4,29). Recently, it was shown that human renal epithelial cells specifically produce the proinflammatory cytokine interleukin-8 in response to F1C fimbria-mediated attachment (4).…”

Section: Strain 83972 Does Not Trigger Host Defense Mechanisms and Lamentioning

confidence: 99%

Mellowing Out: Adaptation to Commensalism by Escherichia coli Asymptomatic Bacteriuria Strain 83972

2007

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Mucosal surfaces in the intestinal, respiratory, and urogenital tracts are populated by a highly diverse bacterial flora. Most host-dwelling bacteria are commensals and maintain a symbiotic relationship with the host; however, a minority are pathogens that attack the mucosa, causing tissue damage and disease symptoms. Bacterial pathogens differ from commensals by the expression of specific virulence factors, such as those that mediate tissue assault. Commensals, in contrast, have generally been regarded as bacteria lacking such virulence factors or other specific mechanisms for interaction with host tissues. Asymptomatic carriage of bacteria may also result after a primary symptomatic infection. However, this type of carrier state differs from commensalism in that variants of pathogenic strains persist without evoking a host response. This review is focused on the molecular basis for attenuation of virulence and adaptation to commensalism, using the prototypic asymptomatic bacteriuria strain Escherichia coli 83972 as a model.Most E. coli strains coexist peacefully with their human host, while others cause disease. E. coli is a versatile pathogen causing a spectrum of diseases, including urinary tract infections (UTIs), diarrhea, sepsis, and meningitis (28). UTIs are among the most common infectious diseases of humans and are a major cause of morbidity. It is estimated that 40 to 50% of healthy adult women have experienced at least one UTI episode (15). Acute pyelonephritis and asymptomatic bacteriuria (ABU) represent the two extremes of UTI. Escherichia coli is responsible for Ͼ80% of UTIs. Acute pyelonephritis is a severe acute systemic infection caused by uropathogenic E. coli (UPEC) clones with virulence genes clustered on "pathogenicity islands" (13,16,25,46,67,72). ABU, on the other hand, is an asymptomatic carrier state that resembles commensalism. Paradoxically, a large proportion of UTIs are caused by ABU E. coli. Individuals infected with ABU group E. coli may carry high urine titers of a single E. coli strain for months or years without provoking a host response. According to conventional notions, pathogens can develop from commensals by the acquisition of virulence-associated genes located on, for example, pathogenicity islands or plasmids. The flip side of this evolutionary force is the equally important adaptation of the newly minted pathogen to its new host niche, where genes are inactivated by either point mutation, insertion, or deletion (39).Here we illustrate such an example, where the commensal-topathogen shift in E. coli is bidirectional. STRAIN 83972 AS A PROPHYLACTIC AGENTE. coli 83972 is a prototype ABU strain and is probably the best-characterized ABU-type E. coli strain to date. It is a clinical isolate capable of long-term bladder colonization. The strain lacks defined O and K surface antigens and is nonmotile (2). Also, electron microscopy of 83972 did not reveal the presence of flagella or a capsule (30, 56). Strain 83972 was originally isolated from a young Swedish girl with ABU who ...

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Receptor Structure for F1C Fimbriae of Uropathogenic Escherichia coli

Cited by 105 publications

References 54 publications

Role of Enterococcus faecalis Surface Protein Esp in the Pathogenesis of Ascending Urinary Tract Infection

Role of Enterococcus faecalis Surface Protein Esp in the Pathogenesis of Ascending Urinary Tract Infection

Evolution of the Chaperone/Usher Assembly Pathway: Fimbrial Classification Goes Greek

Mellowing Out: Adaptation to Commensalism by Escherichia coli Asymptomatic Bacteriuria Strain 83972

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