The effects of extracellular slime from Staphylococcus epidermidis on phagocytic ingestion and killing

Rodgers, J

doi:10.1016/0928-8244(94)90063-9

Cited by 14 publications

(14 citation statements)

References 12 publications

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“…Beginning in the 1980s, several reports were published providing evidence for that function [28–30]. Recent research has given more mechanistic insight, showing that S. epidermidis biofilms protect from neutrophil-dependent killing by complement inactivation via prevention of the deposition of C3b and immunoglobulin G (IgG) [31].…”

Section: Virulence Factors Of S Epidermidismentioning

confidence: 99%

Molecular basis of Staphylococcus epidermidis infections

Otto¹

2011

Semin Immunopathol

215

197

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Staphylococcus epidermidis is the most important member of the coagulase-negative staphylococci and one of the most abundant colonizers of human skin. While for a long time regarded as innocuous, it has been identified as the most frequent cause of device-related infections occurring in the hospital setting and is therefore now recognized as an important opportunistic pathogen. S. epidermidis produces a series of molecules that provide protection from host defenses. Specifically, many proteins and exopolymers, such as the exopolysaccharide PIA, contribute to biofilm formation and inhibit phagocytosis and the activity of human antimicrobial peptides. Furthermore, recent research has identified a family of pro-inflammatory peptides in S. epidermidis, the phenol-soluble modulins (PSMs), which have multiple functions in immune evasion and biofilm development, and may be cytolytic. However, in accordance with the relatively benign relationship that S. epidermidis has with its host, production of aggressive members of the PSM family is kept at a low level. Interestingly, in contrast to Staphylococcus aureus with its large arsenal of toxins developed for causing infection in the human host, most if not all “virulence factors” of S. epidermidis appear to have original functions in the commensal lifestyle of this bacterium.

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Section: Virulence Factors Of S Epidermidismentioning

confidence: 99%

Molecular basis of Staphylococcus epidermidis infections

Otto¹

2011

Semin Immunopathol

215

197

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“…Once bound to the biomaterial, the second step involves the formation of bio®lm. Bio®lm, or its components, have been shown to protect S. epidermidis from antibiotics [37,45], phagocytes [14,38] and inhibit other immune-related activities [10,42]. The end result is that the bacteria are allowed to persist and be shed into the blood for prolonged periods of time.…”

Section: Introductionmentioning

confidence: 99%

Interaction of Staphylococcus epidermidis with endothelial cells in vitro

Merkel

Scofield

2001

Med Microbiol Immunol

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Staphylococcus epidermidis is a leading cause of nosocomial bacteremia, yet virtually nothing is known about how this pathogen interacts with human endothelial cells. We present evidence here that two biofilm-producing strains of S. epidermidis adhere to two types of endothelial cell lines in vitro and that adherence is significantly increased after briefly heat-treating the bacteria at 40 degrees C in the presence of calcium. This mild heat treatment resulted in bacteria that were 5 to more than 20 times more adherent than untreated controls. While the adherence of bacteria in all phases of growth was increased after heat treatment, heat-treated late stationary phase cells were generally the most adherent. Electron microscopy demonstrated that S. epidermidis was internalized and appeared to exist free in the cytoplasm. Adherence to endothelium, should it occur in vivo during bacteremia, may be a virulence factor associated with this bacterium's pathogenesis.

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“…Biofilms are highdensity bacterial consortia, adherent to a surface, in which bacteria are embedded in a heterogeneous bacterium-derived matrix. Early studies already found evidence that biofilm-forming S. epidermidis strains are less susceptible to host innate immune effector mechanisms than non-biofilm-forming strains (19,32,33). It is assumed that in conjunction with the severely reduced susceptibility of biofilm-forming S. epidermidis to antimicrobials, immune escape mechanisms contribute essentially to the chronic persistent course of implant-associated S. epidermidis infections (6,36).…”

mentioning

confidence: 99%

Staphylococcus epidermidis Uses Distinct Mechanisms of Biofilm Formation To Interfere with Phagocytosis and Activation of Mouse Macrophage-Like Cells 774A.1

et al. 2011

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Assembly of adherent biofilms is the key mechanism involved in Staphylococcus epidermidis virulence during device-associated infections. Aside from polysaccharide intercellular adhesin (PIA), the accumulation-associated protein Aap and the extracellular matrix binding protein Embp act as intercellular adhesins, mediating S. epidermidis cell aggregation and biofilm accumulation. The aim of this study was to investigate structural features of PIA-, Aap-, and Embp-mediated S. epidermidis biofilms in more detail and to evaluate their specific contributions to biofilm-related S. epidermidis immune escape. PIA-, Embp-, and Aap-mediated biofilms exhibited substantial morphological differences. Basically, PIA synthesis induced formation of macroscopically visible, rough cell clusters, whereas Aap-and Embp-dependent biofilms preferentially displayed a smooth layer of aggregated bacteria. On the microscopic level, PIA was found to form a string-like organized extracellular matrix connecting the bacteria, while Embp produced small deposits of intercellular matrix and Aap was strictly localized to the bacterial surface. Despite marked differences, S. epidermidis strains using PIA, Aap, or Embp for biofilm formation were protected from uptake by J774A.1 macrophages, with similarly efficiencies. In addition, compared to biofilm-negative S. epidermidis strains, isogenic biofilm-forming S. epidermidis induced only a diminished inflammatory J774A.1 macrophage response, leading to significantly (88.2 to 88.7%) reduced NF-B activation and 68.8 to 83% reduced interleukin-1␤ (IL-1␤) production. Mechanical biofilm dispersal partially restored induction of NF-B activation, although bacterial cell surfaces remained decorated with the respective intercellular adhesins. Our results demonstrate that distinct S. epidermidis biofilm morphotypes are similarly effective at protecting S. epidermidis from phagocytic uptake and at counteracting macrophage activation, providing novel insights into mechanisms that could contribute to the chronic and persistent course of biofilm-related S. epidermidis foreign material infections.

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The effects of extracellular slime from Staphylococcus epidermidis on phagocytic ingestion and killing

Cited by 14 publications

References 12 publications

Molecular basis of Staphylococcus epidermidis infections

Molecular basis of Staphylococcus epidermidis infections

Interaction of Staphylococcus epidermidis with endothelial cells in vitro

Staphylococcus epidermidis Uses Distinct Mechanisms of Biofilm Formation To Interfere with Phagocytosis and Activation of Mouse Macrophage-Like Cells 774A.1

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