Does aggregation substance ofEnterococcus faecalis contribute to development of endocarditis?

Berti, Marisa; Candiani, Gianpaolo; Kaufhold, Achim; Muscholl, Albrecht; Wirth, Reinhard

doi:10.1007/bf02768756

Cited by 21 publications

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“…Another study with the rabbit model of enterococcal endocarditis also documented that the presence of the AS in combination with the expression of the enterococcal binding substance caused high mortality (26). In other animal models (experimental endocarditis and experimental endophthalmitis), the AS had no influence on the outcome of the infections (3,14). These experimental models, however, do not reflect a situation where the enterococci have to adhere to intestinal epithelia and translocate through the mucosa.…”

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Aggregation Substance Increases Adherence and Internalization, but Not Translocation, of Enterococcus faecalis through Different Intestinal Epithelial Cells In Vitro

et al. 2000

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The aggregation substance of Enterococcus faecalis increased bacterial adherence to and internalization by epithelial cells originating from the colon and duodenum but not by cells derived from the ileum. However, enterococcal translocation through monolayers of intestinal epithelium was not observed.Enterococcus faecalis, a gram-positive facultative anaerobic bacterium, belongs to the normal flora of the intestinal tract and is also found in the vaginal vault and the oral cavity. Enterococci have increasingly gained attention as pathogens, since they have become the fourth leading cause of nosocomial infections in the United States (8). E. faecalis frequently causes local or systemic infections, such as urinary tract and abdominal infections, wound infections, bacteremia, and endocarditis (15). It is assumed that many enterococcal infections are endogenous, resulting from bacterial translocation from the intestinal lumen to extraintestinal sites (16,31).Surprisingly little is known about the virulence factors of E. faecalis. One of the potential virulence factors is the aggregation substance (AS), an adhesin encoded by inducible sex pheromone plasmids (for a review, see reference 5). The AS, a signal peptide-containing protein, appears as a hair-like structure on the cell surface and is incorporated primarily into the ''old'' parts of the cell wall (30). It has been demonstrated that this adhesin is responsible for bacterium-bacterium contact during conjugative transfer of sex pheromone plasmids (5).The AS contains two Arg-Gly-Asp motifs which are known to be recognized by integrins, a family of eukaryotic cell surface receptors (24). Since integrins have been reported to be expressed on intestinal epithelial cells (2), we hypothesized that the AS promotes adherence and possibly invasion into these cells, thereby enabling enterococci to translocate through the intestinal epithelial barrier.(This work was presented in part at the 98th General Meeting of the American Society for Microbiology, Atlanta, Ga., 17 to 21 May 1998.)Three different E. faecalis strains (Table 1), kindly provided by R. Wirth (Institute of Microbiology, University of Regensburg, Regensburg, Germany), were used to study the effect of the AS on adherence, internalization, and translocation through intestinal epithelial cells. The bacteria were cultured in Todd-Hewitt medium (Difco, Augsburg, Germany) supplemented with erythromycin (20 g/ml) for growth of the plasmid-containing strains (OG1X/pAM721 and OG1X/pAM944). Since E. faecalis strains expressing the AS spontaneously clump, all inocula were sonicated (Branson W-450 Sonifier; 80 W, 20 s, continuously) to obtain single-cell suspensions. Salmonella enterica serovar Typhimurium ATCC 14028 and Escherichia coli HB101 grown in Luria-Bertani medium were used as positive and negative controls, respectively. For the experiments described below, the bacteria were harvested in mid-log phase and suspended in tissue culture medium without supplements, which served as the infection medium. Appropriate ...

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Aggregation Substance Increases Adherence and Internalization, but Not Translocation, of Enterococcus faecalis through Different Intestinal Epithelial Cells In Vitro

et al. 2000

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“…Results from our laboratory with E. faecalis containing variants of pCF10 (45) also supported these findings in that AS both increased the size of vegetations and increased mortality. However, Berti et al (5) used a rat endocarditis model with pAD1 derivatives and concluded that AS had no significant influence on the virulence of the organism. Inducible expression of AS alone in a heterologous host (Lactococcus lactis) has provided evidence for increased binding to fibrin as well as elevated cell surface hydrophobicity (20).…”

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Antibodies to a Surface-Exposed, N-terminal Domain of Aggregation Substance Are Not Protective in the Rabbit Model of Enterococcus faecalis Infective Endocarditis

et al. 2001

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The aggregation substance (AS) surface protein from Enterococcus faecalis has been implicated as an important virulence factor for the development of infective endocarditis. To evaluate the role of antibodies specific for Asc10 (the AS protein from the conjugative plasmid pCF10) in protective immunity to infective endocarditis, an N-terminal region of Asc10 lacking the signal peptide and predicted to be surface exposed (amino acids 44 to 331; AS 44-331 ) was cloned with a C-terminal histidine tag translational fusion and expressed from Escherichia coli. N-terminal amino acid sequencing of the purified protein revealed the correct sequence, and rabbit polyclonal antisera raised against AS 44-331 reacted specifically to Asc10 expressed from E. faecalis OG1SSp, but not to other proteins as judged by Western blot analysis. Using these antisera, flow cytometry analysis demonstrated that antibodies to AS 44-331 bound to a surface-exposed region of Asc10. Furthermore, antibodies specific for AS 44-331 were opsonic for E. faecalis expressing Asc10 in vitro but not for cells that did not express Asc10. New Zealand White rabbits immunized with AS 44-331 were challenged intravenously with E. faecalis cells constitutively expressing Asc10 in the rabbit model of experimental endocarditis. Highly immune animals did not show significant differences in clearance of organisms from the blood or spleen or in formation of vegetations on the aortic valve, in comparison with nonimmune animals. Although in vivo expression of Asc10 was demonstrated by immunohistochemistry, these experiments provide evidence that immunity to Asc10 does not play a role in protection from experimental infective endocarditis due to E. faecalis and may have important implications for the development of immunological approaches to combat enterococcal endocarditis.

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“…However, in a rabbit model of endocarditis, a disease in which vegetations of platelets and fibrin resulting from bacterial infection are associated with inflammation of the heart valves and lining, aggregation substance from both pAD1 and pCF10 caused an increase in the size of cardiac vegetations (88, 90, 129). No effect of aggregation substance on vegetation size was observed in a rat endocarditis model (138), suggesting that the effects of aggregation substance on pathogenesis may be species or model-specific. The role of aggregation substance in an infection may be to promote the formation of a quorum of cells in a localized microenvironment through clumping, which could affect the expression of factors now known to be quorum regulated, such as the cytolysin (139).…”

Section: Virulence Plasmids In Enterococcus Faecalismentioning

confidence: 97%

Virulence Plasmids of Nonsporulating Gram-Positive Pathogens

Tyne

Gilmore

2014

Microbiol Spectr

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SUMMARY Gram-positive bacteria are leading causes of many types of human infection, including pneumonia, skin and nasopharyngeal infections, as well as urinary tract and surgical wound infections among hospitalized patients. These infections have become particularly problematic because many of the species causing them have become highly resistant to antibiotics. The role of mobile genetic elements, such as plasmids, in the dissemination of antibiotic resistance among Gram-positive bacteria has been well studied; less well understood is the role of mobile elements in the evolution and spread of virulence traits among these pathogens. While these organisms are leading agents of infection, they are also prominent members of the human commensal ecology. It appears that these bacteria are able to take advantage of the intimate association between host and commensal, via virulence traits that exacerbate infection and cause disease. However, evolution into an obligate pathogen has not occurred, presumably because it would lead to rejection of pathogenic organisms from the host ecology. Instead, in organisms that exist as both commensal and pathogen, selection has favored the development of mechanisms for variability. As a result, many virulence traits are localized on mobile genetic elements, such as virulence plasmids and pathogenicity islands. Virulence traits may occur within a minority of isolates of a given species, but these minority populations have nonetheless emerged as a leading problem in infectious disease. This chapter reviews virulence plasmids in nonsporulating Gram-positive bacteria, and examines their contribution to disease pathogenesis.

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Does aggregation substance ofEnterococcus faecalis contribute to development of endocarditis?

Cited by 21 publications

References 34 publications

Aggregation Substance Increases Adherence and Internalization, but Not Translocation, of Enterococcus faecalis through Different Intestinal Epithelial Cells In Vitro

Aggregation Substance Increases Adherence and Internalization, but Not Translocation, of Enterococcus faecalis through Different Intestinal Epithelial Cells In Vitro

Antibodies to a Surface-Exposed, N-terminal Domain of Aggregation Substance Are Not Protective in the Rabbit Model of Enterococcus faecalis Infective Endocarditis

Virulence Plasmids of Nonsporulating Gram-Positive Pathogens

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