scholarly journals Molecular Basis for Preferential Protective Efficacy of Antibodies Directed to the Poorly Acetylated Form of Staphylococcal Poly-N-Acetyl-β-(1-6)-Glucosamine

2007 ◽  
Vol 75 (7) ◽  
pp. 3406-3413 ◽  
Author(s):  
Nuno Cerca ◽  
Kimberly K. Jefferson ◽  
Tomas Maira-Litrán ◽  
Danielle B. Pier ◽  
Casie Kelly-Quintos ◽  
...  
Keyword(s):  
Staphylococcus Epidermidis ◽  
Biofilm Formation ◽  
Molecular Basis ◽  
Protective Efficacy ◽  
Human Monoclonal Antibody ◽  
Protective Activity ◽  
Survival Capacity ◽  
Vaccine Potential ◽  
Surface Polysaccharide ◽  
Overexpressing Strain

ABSTRACT Poly-N-acetyl-glucosamine (PNAG) is a staphylococcal surface polysaccharide influencing biofilm formation that is also under investigation for its vaccine potential. Antibodies that bind to PNAG with either low (<15%) or high (>90%) levels of acetate are superior at opsonic and protective activity compared with antibodies that bind to PNAG with only high levels (>70%) of acetate. PNAG is synthesized by four proteins encoded within the intercellular adhesin (ica) locus icaADBC. In Staphylococcus epidermidis, icaB encodes a deacetylase needed for the surface retention of PNAG and optimal biofilm formation. In this study, we confirmed that icaB plays a similar role in Staphylococcus aureus and found that an icaB mutant of S. aureus expressed significantly less surface-associated PNAG, was highly susceptible to antibody-independent opsonic killing that could not be enhanced with antibody raised against deacetylated PNAG (dPNAG), and had reduced survival capacity in a murine model of bacteremia. In contrast, an icaB-overexpressing strain produced primarily surface-associated PNAG, was more susceptible to opsonophagocytosis with antibody to dPNAG, and had increased survival in a murine bacteremia model. The highly acetylated secreted PNAG was more effective at blocking opsonic killing mediated by a human monoclonal antibody (mAb) to native PNAG than it was at blocking killing mediated by a human mAb to dPNAG, which by itself was a more effective opsonin. Retention of dPNAG on the surface of S. aureus is key to increased survival during bacteremia and also provides a molecular mechanism explaining the superior opsonic and protective activity of antibody to dPNAG.

scholarly journals Differential Roles of Poly-N-Acetylglucosamine Surface Polysaccharide and Extracellular DNA in Staphylococcus aureus and Staphylococcus epidermidis Biofilms

2007 ◽  
Vol 74 (2) ◽  
pp. 470-476 ◽  
Author(s):  
Era A. Izano ◽  
Matthew A. Amarante ◽  
William B. Kher ◽  
Jeffrey B. Kaplan
Keyword(s):  
Staphylococcus Aureus ◽  
Staphylococcus Epidermidis ◽  
Biofilm Formation ◽  
Cetylpyridinium Chloride ◽  
Microtiter Plate ◽  
Dnase I ◽  
Extracellular Dna ◽  
Human Pathogens ◽  
Microtiter Plate Assay ◽  
Surface Polysaccharide

ABSTRACT Staphylococcus aureus and Staphylococcus epidermidis are major human pathogens of increasing importance due to the dissemination of antibiotic-resistant strains. Evidence suggests that the ability to form matrix-encased biofilms contributes to the pathogenesis of S. aureus and S. epidermidis. In this study, we investigated the functions of two staphylococcal biofilm matrix polymers: poly-N-acetylglucosamine surface polysaccharide (PNAG) and extracellular DNA (ecDNA). We measured the ability of a PNAG-degrading enzyme (dispersin B) and DNase I to inhibit biofilm formation, detach preformed biofilms, and sensitize biofilms to killing by the cationic detergent cetylpyridinium chloride (CPC) in a 96-well microtiter plate assay. When added to growth medium, both dispersin B and DNase I inhibited biofilm formation by both S. aureus and S. epidermidis. Dispersin B detached preformed S. epidermidis biofilms but not S. aureus biofilms, whereas DNase I detached S. aureus biofilms but not S. epidermidis biofilms. Similarly, dispersin B sensitized S. epidermidis biofilms to CPC killing, whereas DNase I sensitized S. aureus biofilms to CPC killing. We concluded that PNAG and ecDNA play fundamentally different structural roles in S. aureus and S. epidermidis biofilms.

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

2020 ◽  
Vol 8 (3) ◽  
pp. 344 ◽  
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.

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

2014 ◽  
Vol 21 (9) ◽  
pp. 1206-1214 ◽  
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.

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

2016 ◽  
Vol 109 (10) ◽  
pp. 1403-1415
Author(s):  
Yongchang Yang ◽  
Xuemei Zhang ◽  
Wenfang Huang ◽  
Yibing Yin
Keyword(s):  
Staphylococcus Epidermidis ◽  
Biofilm Formation

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

2001 ◽  
Vol 69 (6) ◽  
pp. 4079-4085 ◽  
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.

scholarly journals Reduced susceptibility to vancomycin and biofilm formation in methicillin-resistant Staphylococcus epidermidis isolated from blood cultures

2014 ◽  
Vol 109 (7) ◽  
pp. 871-878 ◽  
Author(s):  
Luiza Pinheiro ◽  
Carla Ivo Brito ◽  
Valéria Cataneli Pereira ◽  
Adilson de Oliveira ◽  
Carlos Henrique Camargo ◽  
...  
Keyword(s):  
Staphylococcus Epidermidis ◽  
Biofilm Formation ◽  
Blood Cultures ◽  
Methicillin Resistant

scholarly journals An 18 kDa Scaffold Protein Is Critical for Staphylococcus epidermidis Biofilm Formation

2015 ◽  
Vol 11 (3) ◽  
pp. e1004735 ◽  
Author(s):  
Rahel Decker ◽  
Christoph Burdelski ◽  
Melanie Zobiak ◽  
Henning Büttner ◽  
Gefion Franke ◽  
...  
Keyword(s):  
Staphylococcus Epidermidis ◽  
Biofilm Formation ◽  
Scaffold Protein

scholarly journals Biofilm-FormingStaphylococcus epidermidisExpressing Vancomycin Resistance Early after Adhesion to a Metal Surface

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Toshiyuki Sakimura ◽  
Shiro Kajiyama ◽  
Shinji Adachi ◽  
Ko Chiba ◽  
Akihiko Yonekura ◽  
...  
Keyword(s):  
Metal Surface ◽  
Staphylococcus Epidermidis ◽  
Biofilm Formation ◽  
Bacterial Count ◽  
Fluorescence Staining ◽  
Biofilm Growth ◽  
Before And After ◽  
Viable Bacteria ◽  
Coverage Rates ◽  
Resistance Expression

We investigated biofilm formation and time of vancomycin (VCM) resistance expression after adhesion to a metal surface inStaphylococcus epidermidis. Biofilm-formingStaphylococcus epidermidiswith a VCM MIC of 1 μg/mL was used. The bacteria were made to adhere to a stainless steel washer and treated with VCM at different times and concentrations. VCM was administered 0, 2, 4, and 8 hours after adhesion. The amount of biofilm formed was evaluated based on the biofilm coverage rates (BCRs) before and after VCM administration, bacterial viability in biofilm was visually observed using the fluorescence staining method, and the viable bacterial count in biofilm was measured. The VCM concentration required to decrease BCR significantly compared with that of VCM-untreated bacteria was 4 μg/mL, even in the 0 hr group. In the 4 and 8 hr groups, VCM could not inhibit biofilm growth even at 1,024 μg/mL. In the 8 hr group, viable bacteria remained in biofilm at a count of 104CFU even at a high VCM concentration (1,024 μg/mL). It was suggested that biofilm-formingStaphylococcus epidermidisexpresses resistance to VCM early after adhesion to a metal surface. Resistance increased over time after adhesion as the biofilm formed, and strong resistance was expressed 4–8 hours after adhesion.

Sign in / Sign up

Export Citation Format

Share Document