<i>Enterococcus faecalis</i>
            Heme-Dependent Catalase

Frankenberg, Lena; Brugna, Myriam; Hederstedt, Lars

doi:10.1128/jb.184.22.6351-6356.2002

Cited by 111 publications

(113 citation statements)

References 27 publications

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“…One difference between the two enterococcal species is that E. faecium is catalase negative and E. faecalis is catalase positive when the organisms are grown on media such as BHI medium containing hematin (14,42). Another difference between E. faecium and E. faecalis is that E. faecalis is capable of respiration.…”

Section: Discussionmentioning

confidence: 99%

Cytotoxicity of Hydrogen Peroxide Produced by Enterococcus faecium

et al. 2004

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Although the opportunistic bacterial pathogen Enterococcus faecium is a leading source of nosocomial infections, it appears to lack many of the overt virulence factors produced by other bacterial pathogens, and the underlying mechanism of pathogenesis is not clear. Using E. faecium-mediated killing of the nematode worm Caenorhabditis elegans as an indicator of toxicity, we determined that E. faecium produces hydrogen peroxide at levels that cause cellular damage. We identified E. faecium transposon insertion mutants with altered C. elegans killing activity, and these mutants were altered in hydrogen peroxide production. Mutation of an NADH oxidase-encoding gene eliminated nearly all NADH oxidase activity and reduced hydrogen peroxide production. Mutation of an NADH peroxidase-encoding gene resulted in the enhanced accumulation of hydrogen peroxide. E. faecium is able to produce hydrogen peroxide by using glycerol-3-phosphate oxidase, and addition of glycerol to the culture medium enhanced the killing of C. elegans. Conversely, addition of glucose, which leads to the down-regulation of glycerol metabolism, prevented both C. elegans killing and hydrogen peroxide production. Lastly, detoxification of hydrogen peroxide either by exogenously added catalase or by a C. elegans transgenic strain overproducing catalase prevented E. faecium-mediated killing. These results suggest that hydrogen peroxide produced by E. faecium has cytotoxic effects and highlight the utility of C. elegans pathogenicity models for identifying bacterial virulence factors.Enterococci are gram-positive bacteria that usually reside in the gastrointestinal tract as commensal organisms, but they are also capable of causing severe infections (18). Enterococci are the third leading source of nosocomial infections, causing endocarditis, peritonitis, bacteremia, and urinary tract infections. Two enterococcal species are responsible for almost all of these infections. According to a 1997 survey, the majority (85 to 90%) of enterococcal infections are caused by Enterococcus faecalis, and the remaining infections are due to Enterococcus faecium (35). However, in certain settings, the frequency of infections due to E. faecium has been increasing in recent years (50). The acquisition of antibiotic resistance is believed to be the major contributing factor for the elevated incidence of E. faecium infections. Approximately one-half of E. faecium clinical isolates are now resistant to vancomycin, while only a small fraction of E. faecalis clinical isolates are vancomycin resistant (50).The mechanism underlying E. faecium pathogenesis is obscure, due in part to the fact that few E. faecium virulencerelated factors have been identified. The esp fm and hyl Efm genes, encoding a surface protein and hyaluronidase, respectively, are more likely to be present in pathogenic E. faecium strains than in strains isolated from healthy individuals (11,45,61). The esp fm gene appears to be located on a pathogenicity island containing genes implicated in virulence, antibiotic...

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Section: Discussionmentioning

confidence: 99%

Cytotoxicity of Hydrogen Peroxide Produced by Enterococcus faecium

et al. 2004

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“…The monofunctional catalases and the catalase-peroxidases contain heme as a prosthetic group. The monofunctional catalase specified by the genome of E. faecalis has been shown to remove H 2 O 2 (259).…”

Section: Detoxification Of Ros In Labmentioning

confidence: 99%

Stress Physiology of Lactic Acid Bacteria

Papadimitriou

Alegría

Bron

et al. 2016

Microbiol Mol Biol Rev

539

404

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SUMMARYLactic acid bacteria (LAB) are important starter, commensal, or pathogenic microorganisms. The stress physiology of LAB has been studied in depth for over 2 decades, fueled mostly by the technological implications of LAB robustness in the food industry. Survival of probiotic LAB in the host and the potential relatedness of LAB virulence to their stress resilience have intensified interest in the field. Thus, a wealth of information concerning stress responses exists today for strains as diverse as starter (e.g.,Lactococcus lactis), probiotic (e.g., severalLactobacillusspp.), and pathogenic (e.g.,EnterococcusandStreptococcusspp.) LAB. Here we present the state of the art for LAB stress behavior. We describe the multitude of stresses that LAB are confronted with, and we present the experimental context used to study the stress responses of LAB, focusing on adaptation, habituation, and cross-protection as well as on self-induced multistress resistance in stationary phase, biofilms, and dormancy. We also consider stress responses at the population and single-cell levels. Subsequently, we concentrate on the stress defense mechanisms that have been reported to date, grouping them according to their direct participation in preserving cell energy, defending macromolecules, and protecting the cell envelope. Stress-induced responses of probiotic LAB and commensal/pathogenic LAB are highlighted separately due to the complexity of the peculiar multistress conditions to which these bacteria are subjected in their hosts. Induction of prophages under environmental stresses is then discussed. Finally, we present systems-based strategies to characterize the “stressome” of LAB and to engineer new food-related and probiotic LAB with improved stress tolerance.

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“…For bacteria that do not synthesize heme, heme acquisition allows them to aerobically respire or activate catalases, which protect against the oxidative burst of host phagocytes (29,129). In this way, heme acquisition provides an advantage during infection.…”

Section: Role Of Heme In Pathogenesismentioning

confidence: 99%

Overcoming the Heme Paradox: Heme Toxicity and Tolerance in Bacterial Pathogens

2010

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Virtually all bacterial pathogens require iron to infect vertebrates. The most abundant source of iron within vertebrates is in the form of heme as a cofactor of hemoproteins. Many bacterial pathogens have elegant systems dedicated to the acquisition of heme from host hemoproteins. Once internalized, heme is either degraded to release free iron or used intact as a cofactor in catalases, cytochromes, and other bacterial hemoproteins. Paradoxically, the high redox potential of heme makes it a liability, as heme is toxic at high concentrations. Although a variety of mechanisms have been proposed to explain heme toxicity, the mechanisms by which heme kills bacteria are not well understood. Nonetheless, bacteria employ various strategies to protect against and eliminate heme toxicity. Factors involved in heme acquisition and detoxification have been found to contribute to virulence, underscoring the physiological relevance of heme stress during pathogenesis. Herein we describe the current understanding of the mechanisms of heme toxicity and how bacterial pathogens overcome the heme paradox during infection.

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Enterococcus faecalis Heme-Dependent Catalase

Cited by 111 publications

References 27 publications

Cytotoxicity of Hydrogen Peroxide Produced by Enterococcus faecium

Cytotoxicity of Hydrogen Peroxide Produced by Enterococcus faecium

Stress Physiology of Lactic Acid Bacteria

Overcoming the Heme Paradox: Heme Toxicity and Tolerance in Bacterial Pathogens

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