Study on pathogenesis of Enterococcus faecalis in urinary tract

Hirose, Takaoki; Kumamoto, Yoshiaki; Tanaka, Nobuyuki; Yoshioka, Migaku; Tsukamoto, Taiji

doi:10.1007/bf00262034

Cited by 18 publications

(10 citation statements)

References 9 publications

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“…The ability of E. faecalis to cause pyelonephritis in an experimental mouse model of infection has been reported elsewhere (8). In these experiments, E. faecalis alone when used to infect the bladders of mice at a concentration of 10 8 CFU caused pyelonephritis in 50% of infected animals after 7 days.…”

Section: Discussionmentioning

confidence: 77%

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

Shankar¹,

Lockatell

Baghdayan³

et al. 2001

Infect Immun

311

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: 77%

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

Shankar¹,

Lockatell

Baghdayan³

et al. 2001

Infect Immun

311

226

View full text Add to dashboard Cite

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“…However, the lack of a robust animal model of enterococcal UTI has impeded the study of this pathogen within the urinary tract. In previously established models of ascending UTIs, E. faecalis fails to establish persistent bladder colonization and primarily displays tropism to the kidneys (21,29,43,56,61,75). The absence of persistent infections in these murine models reflects the profile of E. faecalis in community-acquired UTIs where this bacterium represents less than 5% of clinical isolates (55).…”

Section: E Faecalis Establishes Persistent Infections In the Bladdersmentioning

confidence: 99%

“…Several rodent models have been developed to study E. faecalis pathogenesis in the urinary tract in single and mixed infections with other Gram-negative pathogens (21,29,43,61,75). These models involve the transurethral inoculation of bacterial suspensions into the bladders of healthy animals or streptozocin-induced diabetic animals (56) and have been shown to be primarily useful for the study of E. faecalis-mediated pyelonephritis.…”

mentioning

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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“…The present studies focused on lipoteichoic acids, cell wall components of gram-positive bacteria, for the following reasons: (1) gram-positive bacteria (e.g., enterococci) are recognized as pathogens in UTI (Hirose et al, 1989;Wells et al, 1990); (2) attachment to epithelial cells, including epithelial cells in the urinary tract, enhances the ability of lipoteichoic acids (LTs) produced by these bacteria to trigger mucosal inflammation (Beachey and Courtney, 1989); (3) under experimental conditions, LTs migrate to areas considerably remote from their site of injection (Leon and Panos, 1987) and accumulate in tissues where they are likely to induce pathogenesis (Hyzy et al, 1992); and (4) repeated administration of LT in vivo has been shown to cause gross morphological changes in the basement membrane of the urothelium and cells in the basal layer of the urothelium (Leon and Panos, 1987).…”

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confidence: 99%

I. A subpopulation of human urothelial cells is stimulated to proliferate by treatment in vitro with lipoteichoic acid, a cell wall component of Streptococcus faecalis

1996

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Urinary tract infection with gram-positive bacteria is common. Avenues for ingress of bacteria into the bladder include luminal and suburothelial infection. Terminally differentiated superficial urothelial cells lining the lumen of the bladder are often shed in response to infection. In contrast, infection-induced altered function of progenitors of urothelial cells residing in the basal layer of the urothelium is likely to have long lasting effects on the structure and function of the urothelium. The main objective of the present studies was to investigate in vitro the possibility that exposure to lipoteichoic acid, a cell wall component of the gram-positive Streptococcus faecalis (LT-2), stimulates basal urothelial cells to proliferate. To simulate conditions that restrict proliferation and inhibit terminal differentiation of urothelial cells in the basal layer, secondary cultures of urothelial cells (UT) were grown on collagen or fibronectin coated substrate in medium containing low levels of Ca2+ (0.2 mM) and growth factors (0.005% bovine pituitary extract [BPE]). Under these conditions, UT cultures displayed a highly reproducible colony size distribution, possibly due to the fact that colonies were progeny of basal cells with various proliferative potentials, retained in vitro. In cultures grown under growth-restricting conditions the majority of progenitors appeared to be quiescent, just like stem cells in the basal layer of the urothelium. Thus, the population of large colonies (more than six cells/colony), was small when a steady state of growth was achieved, 3-7 days after seeding. Growth factors (0.005-0.5% BPE) caused a dose-dependent increase in this population of large colonies. Moreover, treatment of UT grown under growth-restricting conditions (0.005% BPE) with LT-2 increased steady-state levels of the population of large colonies to levels obtained in cultures growing under optimal conditions with respect to growth factors. These results indicated that the subpopulation of progenitors, quiescent under normal conditions, could be stimulated to proliferate. Two lines of evidence were consistent with the possibility that treatment with LT-2 stimulated proliferation of the subpopulation of progenitors and that large colonies were the progeny of this subpopulation of single cells: (1) treatment with LT-2 increased the percentage of single cells that incorporated bromodeoxyuridine (i.e., proliferated) in a time-dependent manner. (2) An increase in the percentage of large colonies was found following LT-2-triggered proliferation of single cells. We propose that, under normal conditions, cells produced in response to LT-2-triggered proliferation of stem cells are removed from the system due to an increased rate of differentiation followed by apoptosis. Recurrent infection and inflammation may not allow these processes to proceed effectively, resulting in chronic injury to the bladder. Moreover, under conditions in which stem cells accumulate mutations that incapacitate their progeny to undergo apoptosis, L...

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Study on pathogenesis of Enterococcus faecalis in urinary tract

Cited by 18 publications

References 9 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

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

I. A subpopulation of human urothelial cells is stimulated to proliferate by treatment in vitro with lipoteichoic acid, a cell wall component of Streptococcus faecalis

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