Evidence that the Enterococcal Polysaccharide Antigen Gene (
 epa
 ) Cluster Is Widespread in
 Enterococcus faecalis
 and Influences Resistance to Phagocytic Killing of
 E. faecalis

Fang, Teng; Jacques-Palaz, Karen; Weinstock, George M.; Murray, Barbara E.

doi:10.1128/iai.70.4.2010-2015.2002

Cited by 87 publications

(115 citation statements)

References 23 publications

(10 reference statements)

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“…1B) (26,27). Since both mutants lack the Epa polysaccharide (20), the different phenotypes suggest that other, as yet undefined differences exist between these mutants. For example, the gene product of orfd4 might be used in other pathways that are important for translocation, and/or some function of orfde6 may be partially complemented in E. faecalis by another gene(s).…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

“…1B) and that is important for virulence in mice and for resistance to phagocytosis and/or killing by polymorphonuclear leukocytes (7,20,(25)(26)(27). The epa gene cluster has been shown to be widespread among E. faecalis strains (20), and Epa is thought to be a species-specific polysaccharide (7). While we have not characterized Epa biochemically, Hancock and Gilmore were able to detect three different cell wall carbohydrates in E. faecalis: a type-specific capsular polysaccharide, a rhamnopolysaccharide (possibly Epa), and a polymer likely representing an integral cell wall teichoic acid (7).…”

Section: Discussionmentioning

confidence: 99%

“…The epa mutants, TX5179 and TX5180 (locations of mutations are shown in Fig. 1B), have previously been shown to be deficient in a major polysaccharide component (20,25) and were grown in BHI broth or agar supplemented with kanamycin at 2,000 g/ml. Escherichia coli DH5␣, a strain previously shown to be unable to translocate Caco-2 monolayers (2), was grown in Luria-Bertani (Difco) broth or agar.…”

Section: Methodsmentioning

confidence: 99%

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Translocation of Enterococcus faecalis Strains across a Monolayer of Polarized Human Enterocyte-Like T84 Cells

Zeng

Fang

Weinstock³

et al. 2004

J Clin Microbiol

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We used a two-chamber system to study transcytosis of Enterococcus faecalis across monolayers of human colon carcinoma-derived T84 cells, which show structural resemblance to the native intestine. Among 16 E. faecalis isolates from different sources, the well-characterized strain OG1RF and 8 other isolates (2 endocarditis isolates, 1 urine isolate, and all 5 fecal isolates) showed translocation in this assay, while 6 clinical isolates (3 endocarditis and 3 urine isolates), the recipient strain JH2-2, and the control, Escherichia coli DH5␣, had no detectable translocation. Of two OG1RF mutants involving the previously studied epa (enterococcal polysaccharide antigen) gene cluster, known to be needed for virulence and resistance to killing by polymorphonuclear leukocytes, one epa mutant (TX5179) was unable to translocate, while TX5180, with an epa disruption farther downstream, showed a moderate decrease in translocation relative to that of the wild-type strain OG1RF (P < 0.01), indicating that the epa gene cluster is important for translocation across a T84 monolayer. This observation was confirmed by complementation of the epa mutant (TX5179) with epa genes and restoration of its translocation ability. In conclusion, we have demonstrated translocation of at least some strains of E. faecalis across T84 monolayers, although strains differ considerably in this ability, and we have demonstrated that epa mutations can cause marked changes in successful translocation. These results suggest that this model may be a useful in vitro system for studying the process of translocation from the intestinal tract.Enterococci are part of the normal flora in human intestines and are also a leading cause of nosocomial infections (5, 12). These organisms seem to be able to migrate from the gastrointestinal tract into the bloodstream and cause systemic infections such as bacteremia and even endocarditis. The passage of bacteria from the gastrointestinal tract to extraintestinal sites is called translocation (1,22). Wells and colleagues have presented evidence that Enterococcus faecalis can translocate across the mouse intestinal tract (23). In their study, following E. faecalis overgrowth (elicited by metronidazole and streptomycin treatment after oral inoculation of E. faecalis resistant to these agents), coccal bacteria appeared in the intestinal lumen and were observed within vacuoles in the cytoplasm of epithelial cells (23). By immunofluorescent microscopy, E. faecalis cells were localized within columnar epithelial cells, lamina propria, submucosa, and muscularis externa. Thus, E. faecalis cells appear to be able to translocate across an intact intestinal tract, although the enterococcal traits involved in the process were not determined. Runkel et al. also reported that morphine, a known inhibitor of myoelectric activity in the intestines of rats that prolongs gut transit time, increases intestinal microflora levels and promotes bacterial translocation from the intestinal tract to extraintestinal sites (16).An in vitro transc...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

Translocation of Enterococcus faecalis Strains across a Monolayer of Polarized Human Enterocyte-Like T84 Cells

Zeng

Fang

Weinstock³

et al. 2004

J Clin Microbiol

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“…Recent studies have demonstrated that the cell wallanchored pheromone-inducible aggregation substance (AS) and the enterococcal polysaccharide antigen (Epa) in E. faecalis are involved in resistance to neutrophil-mediated killing (73)(74)(75). However, the E. faecalis OG1RF strain used in the present study does not bear AS, arguing for alternative mechanisms of immune evasion, such as the downregulation of integrin 4 expression on the surface of neutrophils (76); alteration of the neutrophil properties rendering them nonresponsive to bacterial infections, as is the case during enterococcal sepsis in thermally injured patients and mice (66,68,69); and survival within immune cells such as macrophages and biofilm formation, which are well-characterized virulence attributes of enterococci (18,(77)(78)(79)(80)(81)(82)(83)(84)(85)(86)(87)(88)(89).…”

Section: Discussionmentioning

confidence: 99%

Enterococcus faecalis Overcomes Foreign Body-Mediated Inflammation To Establish Urinary Tract Infections

et al. 2013

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Urinary catheterization elicits major histological and immunological changes that render the bladder susceptible to microbial invasion, colonization, and dissemination. However, it is not understood how catheters induce these changes, how these changes act to promote infection, or whether they may have any protective benefit. In the present study, we examined how catheter-associated inflammation impacts infection by Enterococcus faecalis, a leading cause of catheter-associated urinary tract infection (CAUTI), a source of significant societal and clinical challenges. Using a recently optimized murine model of foreign body-associated UTI, we found that the implanted catheter itself was the primary inducer of inflammation. In the absence of the silicone tubing implant, E. faecalis induced only minimal inflammation and was rapidly cleared from the bladder. The catheter-induced inflammation was only minimally altered by subsequent enterococcal infection and was not suppressed by inhibitors of the neurogenic pathway and only partially by dexamethasone. Despite the robust inflammatory response induced by urinary implantation, E. faecalis produced biofilm and high bladder titers in these animals. Induction of inflammation in the absence of an implanted catheter failed to promote infection, suggesting that the presence of the catheter itself is essential for E. faecalis persistence in the bladder. Immunosuppression prior to urinary catheterization enhanced E. faecalis colonization, suggesting that implant-mediated inflammation contributes to the control of enterococcal infection. Thus, this study underscores the need for novel strategies against CAUTIs that seek to reduce the deleterious effects of implant-mediated inflammation on bladder homeostasis while maintaining an active immune response that effectively limits bacterial invaders. U rinary catheterization is directly associated with 80% of hospital-acquired urinary tract infections (UTIs) (1). The insertion and presence of indwelling urinary catheters disrupt the normal mechanical and host defenses of the urinary tract, allow extracellular microbes access to the sterile environment of the bladder by ascending through the catheter lumen or from the urethral meatus along the catheter, and provide an additional surface for biofilm formation and the establishment of antibioticrecalcitrant chronic or recurrent infections (2-9). Even in the absence of microbial colonization, urinary catheterization was shown to be associated with histological and immunological alterations in the bladder, including urothelial damage and exfoliation, bladder wall edema, inflammatory cytokine production, immune cell infiltration, and mucosal lesions of the bladders and kidneys (7, 10-13) which can lead to bladder cancers (14, 15). However, there remains a need to uncover molecular details and the functional role of the catheter-induced host responses during bacterial colonization and catheter-associated UTIs (CAUTIs).We recently optimized a murine model of foreign body-associated UTI to inv...

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Enterococcus

Teixeira¹,

Facklam²

2010

Topley &Amp; Wilson's Microbiology and Microbial Infections

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Evidence that the Enterococcal Polysaccharide Antigen Gene ( epa ) Cluster Is Widespread in Enterococcus faecalis and Influences Resistance to Phagocytic Killing of E. faecalis

Cited by 87 publications

References 23 publications

Translocation of Enterococcus faecalis Strains across a Monolayer of Polarized Human Enterocyte-Like T84 Cells

Translocation of Enterococcus faecalis Strains across a Monolayer of Polarized Human Enterocyte-Like T84 Cells

Enterococcus faecalis Overcomes Foreign Body-Mediated Inflammation To Establish Urinary Tract Infections

Enterococcus

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