Structural basis of Staphylococcus epidermidis biofilm formation: mechanisms and molecular interactions

Objectives This study aims to examine biofilm formed on vascular prostheses by Staphylococcus epidermidis with different ica and aap genetic status, and to evaluate the effect of antibiotic-modified prostheses on bacterial colonization. Methods Biofilm formation was determined using fluorescence microscopy imaging. Quantitative analysis was conducted using the biofilm coverage ratio (BCR) calculations. Results Our investigations prove that the BCR method with fluorescent dye enabled an accurate assessment of biofilm coverage and comparison of the obtained results. The ica+ aap+ strains formed a biofilm on all of the examined vascular prostheses. Uni-Graft® modified with covalently immobilized amikacin was effective in preventing bacterial adherence. Conclusions Molecular biology techniques combined with phenotype studies give a broad insight into biofilm formation mechanisms. On the other hand, fluorescence microscopy imaging along with BCR calculations are reliable and simple tools to quantitatively estimate biofilm formation, as well as the effectiveness of antimicrobial prosthesis modification.

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Fighting Staphylococcus epidermidis Biofilm-Associated Infections: Can Iron Be the Key to Success?

Frontiers in Cellular and Infection Microbiology ◽

10.3389/fcimb.2021.798563 ◽

2021 ◽

Vol 11 ◽

Author(s):

Fernando Oliveira ◽

Holger Rohde ◽

Manuel Vilanova ◽

Nuno Cerca

Keyword(s):

Iron Metabolism ◽

Staphylococcus Epidermidis ◽

Biofilm Formation ◽

Iron Acquisition ◽

Bacterial Species ◽

Multidrug Resistant ◽

Formation Mechanisms ◽

Bacterial Genes ◽

Amount Of Knowledge ◽

Biofilm Development

Staphylococcus epidermidis is one of the most important commensal microorganisms of human skin and mucosae. However, this bacterial species is also the cause of severe infections in immunocompromised patients, specially associated with the utilization of indwelling medical devices, that often serve as a scaffold for biofilm formation. S. epidermidis strains are often multidrug resistant and its association with biofilm formation makes these infections hard to treat. Their remarkable ability to form biofilms is widely regarded as its major pathogenic determinant. Although a significant amount of knowledge on its biofilm formation mechanisms has been achieved, we still do not understand how the species survives when exposed to the host harsh environment during invasion. A previous RNA-seq study highlighted that iron-metabolism associated genes were the most up-regulated bacterial genes upon contact with human blood, which suggested that iron acquisition plays an important role in S. epidermidis biofilm development and escape from the host innate immune system. In this perspective article, we review the available literature on the role of iron metabolism on S. epidermidis pathogenesis and propose that exploiting its dependence on iron could be pursued as a viable therapeutic alternative.

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Lucilia sericata Chymotrypsin Disrupts Protein Adhesin-Mediated Staphylococcal Biofilm Formation

Applied and Environmental Microbiology ◽

10.1128/aem.03689-12 ◽

2012 ◽

Vol 79 (4) ◽

pp. 1393-1395 ◽

Cited By ~ 35

Author(s):

Llinos G. Harris ◽

Yamni Nigam ◽

James Sawyer ◽

Dietrich Mack ◽

David I. Pritchard

Keyword(s):

Staphylococcus Aureus ◽

Staphylococcus Epidermidis ◽

Biofilm Formation ◽

Lucilia Sericata ◽

Bacterial Biofilm ◽

Bacterial Biofilms ◽

Formation Mechanisms ◽

Chronic Infections ◽

Content Type ◽

Effective Activity

ABSTRACTStaphylococcus aureusandStaphylococcus epidermidisbiofilms cause chronic infections due to their ability to form biofilms. The excretions/secretions ofLucilia sericatalarvae (maggots) have effective activity for debridement and disruption of bacterial biofilms. In this paper, we demonstrate how chymotrypsin derived from maggot excretions/secretions disrupts protein-dependent bacterial biofilm formation mechanisms.

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Transporters and Efflux Pumps Are the Main Mechanisms Involved in Staphylococcus epidermidis Adaptation and Tolerance to Didecyldimethylammonium Chloride

Microorganisms ◽

10.3390/microorganisms8030344 ◽

2020 ◽

Vol 8 (3) ◽

pp. 344 ◽

Cited By ~ 1

Author(s):

Urška Ribič ◽

Jernej Jakše ◽

Nataša Toplak ◽

Simon Koren ◽

Minka Kovač ◽

...

Keyword(s):

Staphylococcus Epidermidis ◽

Biofilm Formation ◽

Efflux Pump ◽

Thioredoxin Reductase ◽

Multidrug Transporter ◽

Acid Biosynthesis ◽

Tolerance Mechanisms ◽

Down Regulation ◽

Didecyldimethylammonium Chloride ◽

First Time

Staphylococcus epidermidis cleanroom strains are often exposed to sub-inhibitory concentrations of disinfectants, including didecyldimethylammonium chloride (DDAC). Consequently, they can adapt or even become tolerant to them. RNA-sequencing was used to investigate adaptation and tolerance mechanisms of S. epidermidis cleanroom strains (SE11, SE18), with S. epidermidis SE11Ad adapted and S. epidermidis SE18To tolerant to DDAC. Adaptation to DDAC was identified with up-regulation of genes mainly involved in transport (thioredoxin reductase [pstS], the arsenic efflux pump [gene ID, SE0334], sugar phosphate antiporter [uhpT]), while down-regulation was seen for the Agr system (agrA, arC, agrD, psm, SE1543), for enhanced biofilm formation. Tolerance to DDAC revealed the up-regulation of genes associated with transporters (L-cysteine transport [tcyB]; uracil permease [SE0875]; multidrug transporter [lmrP]; arsenic efflux pump [arsB]); the down-regulation of genes involved in amino-acid biosynthesis (lysine [dapE]; histidine [hisA]; methionine [metC]), and an enzyme involved in peptidoglycan, and therefore cell wall modifications (alanine racemase [SE1079]). We show for the first time the differentially expressed genes in DDAC-adapted and DDAC-tolerant S. epidermidis strains, which highlight the complexity of the responses through the involvement of different mechanisms.

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A Single B-Repeat of Staphylococcus epidermidis Accumulation-Associated Protein Induces Protective Immune Responses in an Experimental Biomaterial-Associated Infection Mouse Model

Clinical and Vaccine Immunology ◽

10.1128/cvi.00306-14 ◽

2014 ◽

Vol 21 (9) ◽

pp. 1206-1214 ◽

Cited By ~ 12

Author(s):

Lin Yan ◽

Lei Zhang ◽

Hongyan Ma ◽

David Chiu ◽

James D. Bryers

Keyword(s):

Staphylococcus Epidermidis ◽

Biofilm Formation ◽

Porous Scaffold ◽

The United States ◽

Protein Vaccine ◽

Weight Changes ◽

Biofilm Inhibition ◽

Content Type ◽

Accumulation Associated Protein

ABSTRACTNosocomial infections are the fourth leading cause of morbidity and mortality in the United States, resulting in 2 million infections and ∼100,000 deaths each year. More than 60% of these infections are associated with some type of biomedical device.Staphylococcus epidermidisis a commensal bacterium of the human skin and is the most common nosocomial pathogen infecting implanted medical devices, especially those in the cardiovasculature.S. epidermidisantibiotic resistance and biofilm formation on inert surfaces make these infections hard to treat. Accumulation-associated protein (Aap), a cell wall-anchored protein ofS. epidermidis, is considered one of the most important proteins involved in the formation ofS. epidermidisbiofilm. A small recombinant protein vaccine comprising a single B-repeat domain (Brpt1.0) ofS. epidermidisRP62A Aap was developed, and the vaccine's efficacy was evaluatedin vitrowith a biofilm inhibition assay andin vivoin a murine model of biomaterial-associated infection. A high IgG antibody response againstS. epidermidisRP62A was detected in the sera of the mice after two subcutaneous immunizations with Brpt1.0 coadministered with Freund's adjuvant. Sera from Brpt1.0-immunized mice inhibitedin vitroS. epidermidisRP62A biofilm formation in a dose-dependent pattern. After receiving two immunizations, each mouse was surgically implanted with a porous scaffold disk containing 5 × 106CFU ofS. epidermidisRP62A. Weight changes, inflammatory markers, and histological assay results after challenge withS. epidermidisindicated that the mice immunized with Brpt1.0 exhibited significantly higher resistance toS. epidermidisRP62A implant infection than the control mice. Day 8 postchallenge, there was a significantly lower number of bacteria in scaffold sections and surrounding tissues and a lower residual inflammatory response to the infected scaffold disks for the Brpt1.0-immunized mice than for of the ovalbumin (Ova)-immunized mice.

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SCCmec-associated psm-mec mRNA promotes Staphylococcus epidermidis biofilm formation

Antonie van Leeuwenhoek ◽

10.1007/s10482-016-0741-2 ◽

2016 ◽

Vol 109 (10) ◽

pp. 1403-1415

Author(s):

Yongchang Yang ◽

Xuemei Zhang ◽

Wenfang Huang ◽

Yibing Yin

Keyword(s):

Staphylococcus Epidermidis ◽

Biofilm Formation

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Anaerobic Conditions Induce Expression of Polysaccharide Intercellular Adhesin in Staphylococcus aureus and Staphylococcus epidermidis

Infection and Immunity ◽

10.1128/iai.69.6.4079-4085.2001 ◽

2001 ◽

Vol 69 (6) ◽

pp. 4079-4085 ◽

Cited By ~ 222

Author(s):

Sarah E. Cramton ◽

Martina Ulrich ◽

Friedrich Götz ◽

Gerd Döring

Keyword(s):

Staphylococcus Aureus ◽

Staphylococcus Epidermidis ◽

Biofilm Formation ◽

Extracellular Polysaccharide ◽

Growth Conditions ◽

Anaerobic Conditions ◽

Anaerobic Environment ◽

Specific Mrna

ABSTRACT Products of the intercellular adhesion (ica) operon in Staphylococcus aureus and Staphylococcus epidermidis synthesize a linear β-1,6-linked glucosaminylglycan. This extracellular polysaccharide mediates bacterial cell-cell adhesion and is required for biofilm formation, which is thought to increase the virulence of both pathogens in association with prosthetic biomedical implants. The environmental signal(s) that triggers ica gene product and polysaccharide expression is unknown. Here we demonstrate that anaerobic in vitro growth conditions lead to increased polysaccharide expression in both S. aureus and S. epidermidis, although the regulation is less stringent inS. epidermidis. Anaerobiosis also dramatically stimulates ica-specific mRNA expression inica- and polysaccharide-positive strains of both S. aureus and S. epidermidis.These data suggest a mechanism whereby ica gene expression and polysaccharide production may act as a virulence factor in an anaerobic environment in vivo.

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