Dynamic interactions between host and pathogen during acute urinary tract infections

Schilling, Joel D.; Mulvey, Matthew A.; Hultgren, Scott J.

doi:10.1016/s0090-4295(01)01130-x

Cited by 58 publications

(38 citation statements)

References 28 publications

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“…However, internalization causes exfoliation of the superficial bladder cells harboring internalized bacteria into the urine. Before clearance, intracellular bacteria start to replicate and induce host cytokine responses, leading to the symptoms of UTI (221,246,305).…”

Section: Uropathogenic E Colimentioning

confidence: 99%

Pathogenicity Islands in BacterialPathogenesis

2004

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In this review, we focus on a group of mobile genetic elements designated pathogenicity islands (PAI). These elements play a pivotal role in the virulence of bacterial pathogens of humans and are also essential for virulence in pathogens of animals and plants. Characteristic molecular features of PAI of important human pathogens and their role in pathogenesis are described. The availability of a large number of genome sequences of pathogenic bacteria and their benign relatives currently offers a unique opportunity for the identification of novel pathogen-specific genomic islands. However, this knowledge has to be complemented by improved model systems for the analysis of virulence functions of bacterial pathogens. PAI apparently have been acquired during the speciation of pathogens from their nonpathogenic or environmental ancestors. The acquisition of PAI not only is an ancient evolutionary event that led to the appearance of bacterial pathogens on a timescale of millions of years but also may represent a mechanism that contributes to the appearance of new pathogens within a human life span. The acquisition of knowledge about PAI, their structure, their mobility, and the pathogenicity factors they encode not only is helpful in gaining a better understanding of bacterial evolution and interactions of pathogens with eukaryotic host cells but also may have important practical implications such as providing delivery systems for vaccination, tools for cell biology, and tools for the development of new strategies for therapy of bacterial infections

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Section: Uropathogenic E Colimentioning

confidence: 99%

Pathogenicity Islands in BacterialPathogenesis

2004

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“…Bacterial cells were collected from overnight cultures by centrifugation at 8,000 ϫ g for 5 min and resuspended in 1ϫ phosphate-buffered saline (1ϫ PBS) to an approximate optical density at 600 nm of 1 corresponding to approximately 7 ϫ 10 8 CFU/ml. Seven-to eightweek-old female C57BL/6Ncr mice with or without a silicone implant were anesthetized by inhalation of isoflurane and infected by transurethral catheterization as previously described (23,44,59) with 50-l inocula of PBS or bacterial suspensions (ϳ2 ϫ 10 7 to 3.5 ϫ 10 7 CFU) immediately following implantation. To quantify bacteria present on implants and in mouse organs, mice were sacrificed at desired time points by cervical dislocation after anesthesia inhalation, and the bladders and kidneys were aseptically harvested.…”

Section: Methodsmentioning

confidence: 99%

Enterococcal Biofilm Formation and Virulence in an Optimized Murine Model of Foreign Body-Associated Urinary Tract Infections

Guiton¹,

Hung²,

et al. 2010

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Catheter-associated urinary tract infections (CAUTIs) constitute the majority of nosocomial UTIs and pose significant clinical challenges. Enterococcal species are among the predominant causative agents of CAUTIs. However, very little is known about the pathophysiology of Enterococcus-mediated UTIs. We optimized a murine model of foreign body-associated UTI in order to mimic conditions of indwelling catheters in patients. In this model, the presence of a foreign body elicits major histological changes and induces the expression of several proinflammatory cytokines in the bladder. In addition, in contrast to naïve mice, infection of catheterimplanted mice with Enterococcus faecalis induced the specific expression of interleukin 1␤ (IL-1␤) and macrophage inflammatory protein 1␣ (MIP-1␣) in the bladder. These responses resulted in a favorable niche for the development of persistent E. faecalis infections in the murine bladders and kidneys. Furthermore, biofilm formation on the catheter implant in vivo correlated with persistent infections. However, the enterococcal autolytic factors GelE and Atn (also known as AtlA), which are important in biofilm formation in vitro, are dispensable in vivo. In contrast, the housekeeping sortase A (SrtA) is critical for biofilm formation and virulence in CAUTIs. Overall, this murine model represents a significant advance in the understanding of CAUTIs and underscores the importance of urinary catheterization during E. faecalis uropathogenesis. This model is also a valuable tool for the identification of virulence determinants that can serve as potential antimicrobial targets for the treatment of enterococcal infections.

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“…Type 1 fimbriae are proinflammatory, stimulating release of IL-6, IL-8, and tumor necrosis factor ␣, and they act synergistically with other bacterial products such as lipopolysaccharide (8)(9)(10)(11)(12). The adhesin is sufficient for invasion of uroepithelial cells and may contribute to the etiology of the chronic inflammatory diseases, Crohn's disease, and interstitial cystitis (13)(14)(15)(16).…”

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confidence: 99%

Integrated regulatory responses of fimB to N -acetylneuraminic (sialic) acid and GlcNAc in Escherichia coli K-12

Sohanpal

El-Labany

Lahooti

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

103

132

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. Here, we show that whereas NanR, a sialic acid-response regulator, binds to region 1, NagC, a GlcNAc-6P-responsive protein, binds to region 2 instead. The NanR-and NagC-binding sites lie adjacent to deoxyadenosine methylase (Dam) methylation sites (5 -GATC) that are protected from modification, and the two regulators are shown to be required for methylation protection at regions 1 and 2, respectively. Mutations in nanR and nagC diminish fimB expression, and both fimB expression and FimB recombination are inhibited by GlcNAc (3-and >35-fold, respectively). Sialic acid catabolism generates GlcNAc-6-P, and whereas GlcNAc disrupts methylation protection by NagC alone, Neu5Ac inhibits the protection mediated by both NanR and NagC as expected. Type 1 fimbriae are proinflammatory, and host defenses enhance the release of both Neu5Ac and GlcNAc by a variety of mechanisms. Inhibition of type 1 fimbriation by these amino sugars may thus help balance the interaction between E. coli and its hosts. type 1 fimbriae

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Dynamic interactions between host and pathogen during acute urinary tract infections

Cited by 58 publications

References 28 publications

Pathogenicity Islands in BacterialPathogenesis

Pathogenicity Islands in BacterialPathogenesis

Enterococcal Biofilm Formation and Virulence in an Optimized Murine Model of Foreign Body-Associated Urinary Tract Infections

Integrated regulatory responses of fimB to N -acetylneuraminic (sialic) acid and GlcNAc in Escherichia coli K-12

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