scholarly journals Nicotine Enhances Staphylococcus epidermidis Biofilm Formation by Altering the Bacterial Autolysis, Extracellular DNA Releasing, and Polysaccharide Intercellular Adhesin Production

2018 ◽  
Vol 9 ◽  
Author(s):  
Yang Wu ◽  
Yue Ma ◽  
Tao Xu ◽  
Qing-zhao Zhang ◽  
Jinna Bai ◽  
...  
Keyword(s):  
Staphylococcus Epidermidis ◽  
Biofilm Formation ◽  
Extracellular Dna ◽  
Polysaccharide Intercellular Adhesin

Transcriptional activity of icaADBC is not correlated to the degree of biofilm formation in clinical ica-positive Staphylococcus epidermidis strains

Biofilms ◽  
2004 ◽  
Vol 1 (2) ◽  
pp. 101-106 ◽  
Author(s):  
S. Dobinsky ◽  
H. Rohde ◽  
J. K.-M. Knobloch ◽  
M. A. Horstkotte ◽  
D. Mack
Keyword(s):  
Sequence Analysis ◽  
Growth Phase ◽  
Staphylococcus Epidermidis ◽  
Biofilm Formation ◽  
Promoter Region ◽  
Transcriptional Activity ◽  
Exponential Growth Phase ◽  
Polysaccharide Intercellular Adhesin ◽  
Different Strains ◽  
Negative Phenotype

Biofilm-formation in Staphylococcus epidermidis depends on the expression of the icaADBC operon encoding the enzymes required for the synthesis of polysaccharide intercellular adhesin (PIA). Different S. epidermidis strains vary widely in the degree of PIA and biofilm that they produce. In 11 clinical S. epidermidis strains we analyzed the biofilm-forming capacity in relation to the amount of ica expressed in static biofilm cultures. In mid-exponential growth phase no correlation could be detected between the level of ica transcription and the biofilm-forming phenotype. When the different strains were grown under conditions leading to a biofilm-negative phenotype, ica-expression was highly upregulated. Sequence analysis demonstrated that the observed differences were not due to major mutations in the ica promoter region but apparently to other strain-specific regulators.

scholarly journals Conversion of Staphylococcus epidermidis Strains from Commensal to Invasive by Expression of the ica Locus Encoding Production of Biofilm Exopolysaccharide

2005 ◽  
Vol 73 (5) ◽  
pp. 3188-3191 ◽  
Author(s):  
Hualin Li ◽  
Lin Xu ◽  
Jianping Wang ◽  
Yumei Wen ◽  
Cuong Vuong ◽  
...  
Keyword(s):  
Central Venous Catheter ◽  
Staphylococcus Epidermidis ◽  
Biofilm Formation ◽  
Venous Catheter ◽  
Infection Model ◽  
Polysaccharide Intercellular Adhesin ◽  
Central Venous ◽  
Biofilm Production ◽  
Central Venous Catheter Infection

ABSTRACT To test if biofilm formation in Staphylococcus epidermidis is dependent on the polysaccharide intercellular adhesin, whose biosynthesis is driven by the ica locus, a plasmid containing the ica locus was transferred to three ica-negative strains. Using in vitro biofilm assays and a rat central venous catheter infection model, we confirmed the importance of the ica locus for biofilm production and pathogenesis of S. epidermidis.

scholarly journals Extracellular DNA Impedes the Transport of Vancomycin in Staphylococcus epidermidis Biofilms Preexposed to Subinhibitory Concentrations of Vancomycin

2014 ◽  
Vol 58 (12) ◽  
pp. 7273-7282 ◽  
Author(s):  
Natalya Doroshenko ◽  
Boo Shan Tseng ◽  
Robert P. Howlin ◽  
Jill Deacon ◽  
Julian A. Wharton ◽  
...  
Keyword(s):  
Confocal Microscopy ◽  
Isothermal Titration Calorimetry ◽  
Staphylococcus Epidermidis ◽  
Binding Constant ◽  
Biofilm Formation ◽  
Potential Role ◽  
Extracellular Dna ◽  
Titration Calorimetry ◽  
Orthopedic Implant ◽  
Content Type

ABSTRACTStaphylococcus epidermidisbiofilm formation is responsible for the persistence of orthopedic implant infections. Previous studies have shown that exposure ofS. epidermidisbiofilms to sub-MICs of antibiotics induced an increased level of biofilm persistence. BODIPY FL-vancomycin (a fluorescent vancomycin conjugate) and confocal microscopy were used to show that the penetration of vancomycin through sub-MIC-vancomycin-treatedS. epidermidisbiofilms was impeded compared to that of control, untreated biofilms. Further experiments showed an increase in the extracellular DNA (eDNA) concentration in biofilms preexposed to sub-MIC vancomycin, suggesting a potential role for eDNA in the hindrance of vancomycin activity. Exogenously added,S. epidermidisDNA increased the planktonic vancomycin MIC and protected biofilm cells from lethal vancomycin concentrations. Finally, isothermal titration calorimetry (ITC) revealed that the binding constant of DNA and vancomycin was 100-fold higher than the previously reported binding constant of vancomycin and its intended cellulard-Ala-d-Ala peptide target. This study provides an explanation of the eDNA-based mechanism of antibiotic tolerance in sub-MIC-vancomycin-treatedS. epidermidisbiofilms, which might be an important factor for the persistence of biofilm infections.

scholarly journals The Teicoplanin-Associated Locus Regulator (TcaR) and the Intercellular Adhesin Locus Regulator (IcaR) Are Transcriptional Inhibitors of the ica Locus in Staphylococcus aureus

2004 ◽  
Vol 186 (8) ◽  
pp. 2449-2456 ◽  
Author(s):  
Kimberly K. Jefferson ◽  
Danielle B. Pier ◽  
Donald A. Goldmann ◽  
Gerald B. Pier
Keyword(s):  
Staphylococcus Aureus ◽  
Staphylococcus Epidermidis ◽  
Biofilm Formation ◽  
Negative Regulator ◽  
Regulatory Proteins ◽  
Polysaccharide Intercellular Adhesin ◽  
Topoisomerase Iv ◽  
Exogenous Factors ◽  
Dna Affinity Chromatography

ABSTRACT Infections involving Staphylococcus aureus are often more severe and difficult to treat when the organism assumes a biofilm mode of growth. The polysaccharide poly-N-acetylglucosamine (PNAG), also known as polysaccharide intercellular adhesin, is synthesized by the products of the intercellular adhesin (ica) locus and plays a key role in biofilm formation. Numerous conditions and exogenous factors influence ica transcription and PNAG synthesis, but the regulatory factors and pathways through which these environmental stimuli act have been only partially characterized. We developed a DNA affinity chromatography system to purify potential regulatory proteins that bind to the ica promoter region. Using this technique, we isolated four proteins, including the staphylococcal gene regulator SarA, a MarR family transcriptional regulator of the teicoplanin-associated locus TcaR, DNA-binding protein II, and topoisomerase IV, that bound to the ica promoter. Site-directed deletion mutagenesis of tcaR indicated that TcaR was a negative regulator of ica transcription, but deletion of tcaR alone did not induce any changes in PNAG production or in adherence to polystyrene. We also investigated the role of IcaR, encoded within the ica locus but divergently transcribed from the biosynthetic genes. As has been shown previously in Staphylococcus epidermidis, we found that IcaR was also a negative regulator of ica transcription in S. aureus. We also demonstrate that mutation of icaR augmented PNAG production and adherence to polystyrene. Transcription of the ica locus, PNAG production, and adherence to polystyrene were further increased in a tcaR icaR double mutant. In summary, TcaR appeared to be a weak negative regulator of transcription of the ica locus, whereas IcaR was a strong negative regulator, and in their absence PNAG production and biofilm formation were enhanced.

scholarly journals Biofilm Formation by Staphylococcus epidermidis Depends on Functional RsbU, an Activator of thesigB Operon: Differential Activation Mechanisms Due to Ethanol and Salt Stress

2001 ◽  
Vol 183 (8) ◽  
pp. 2624-2633 ◽  
Author(s):  
Johannes K.-M. Knobloch ◽  
Katrin Bartscht ◽  
Axel Sabottke ◽  
Holger Rohde ◽  
Heinz-Hubert Feucht ◽  
...  
Keyword(s):  
Staphylococcus Epidermidis ◽  
Biofilm Formation ◽  
Fragment Length Polymorphism ◽  
Insertion Site ◽  
Alternative Sigma Factor ◽  
Polysaccharide Intercellular Adhesin ◽  
Wild Type ◽  
Activation Mechanisms ◽  
Pathogenetic Factor ◽  
Negative Phenotype

ABSTRACT Staphylococcus epidermidis is a common pathogen in medical device-associated infections. Its major pathogenetic factor is the ability to form adherent biofilms. The polysaccharide intercellular adhesin (PIA), which is synthesized by the products of theicaADBC gene cluster, is essential for biofilm accumulation. In the present study, we characterized the gene locus inactivated by Tn917 insertions of two isogenic,icaADBC-independent, biofilm-negative mutants, M15 and M19, of the biofilm-producing bacterium S. epidermidis 1457. The insertion site was the same in both of the mutants and was located in the first gene, rsbU, of an operon highly homologous to thesigB operons of Staphylococcus aureus andBacillus subtilis. Supplementation of Trypticase soy broth with NaCl (TSBNaCl) or ethanol (TSBEtOH), both of which are known activators of sigB, led to increased biofilm formation and PIA synthesis by S. epidermidis 1457. Insertion of Tn917 into rsbU, a positive regulator of alternative sigma factor ςB, led to a biofilm-negative phenotype and almost undetectable PIA production. Interestingly, in TSBEtOH, the mutants were enabled to form a biofilm again with phenotypes similar to those of the wild type. In TSBNaCl, the mutants still displayed a biofilm-negative phenotype. No difference in primary attachment between the mutants and the wild type was observed. Similar phenotypic changes were observed after transfer of the Tn917 insertion of mutant M15 to the independent and biofilm-producing strain S. epidermidis8400. In 11 clinical S. epidermidis strains, a restriction fragment length polymorphism of the sigB operon was detected which was independent of the presence of theicaADBC locus and a biofilm-positive phenotype. Obviously, different mechanisms are operative in the regulation of PIA expression in stationary phase and under stress induced by salt or ethanol.

scholarly journals Biofilm Formation, icaADBC Transcription, and Polysaccharide Intercellular Adhesin Synthesis by Staphylococci in a Device-Related Infection Model

2005 ◽  
Vol 73 (3) ◽  
pp. 1811-1819 ◽  
Author(s):  
Ursula Fluckiger ◽  
Martina Ulrich ◽  
Andrea Steinhuber ◽  
Gerd Döring ◽  
Dietrich Mack ◽  
...  
Keyword(s):  
Staphylococcus Epidermidis ◽  
Biofilm Formation ◽  
Anaerobic Growth ◽  
Infection Model ◽  
Transcript Analysis ◽  
Polysaccharide Intercellular Adhesin ◽  
Wild Type ◽  
Type Strains

ABSTRACT Biofilm formation of Staphylococcus epidermidis and S. aureus is mediated by the polysaccharide intercellular adhesin (PIA) encoded by the ica operon. We used a device-related animal model to investigate biofilm formation, PIA expression (immunofluorescence), and ica transcription (quantitative transcript analysis) throughout the course of infection by using two prototypic S. aureus strains and one S. epidermidis strain as well as corresponding ica mutants. During infection, the ica mutants were growth attenuated when inoculated in competition with the corresponding wild-type strains but not when grown singly. A typical biofilm was observed at the late course of infection. Only in S. aureus RN6390, not in S. aureus Newman, were PIA and ica-specific transcripts detectable after anaerobic growth in vitro. However, both S. aureus strains were PIA positive in vivo by day 8 of infection. ica transcription preceded PIA expression and biofilm formation in vivo. In S. epidermidis, both PIA and ica expression levels were elevated compared to those in the S. aureus strains in vitro as well as in vivo and were detectable throughout the course of infection. In conclusion, in S. aureus, PIA expression is dependent on the genetic background of the strain as well as on strong inducing conditions, such as those dominating in vivo. In S. epidermidis, PIA expression is elevated and less vulnerable to environmental conditions.

scholarly journals Essential Functional Role of the Polysaccharide Intercellular Adhesin of Staphylococcus epidermidis in Hemagglutination

1999 ◽  
Vol 67 (2) ◽  
pp. 1004-1008 ◽  
Author(s):  
Dietrich Mack ◽  
Joachim Riedewald ◽  
Holger Rohde ◽  
Tim Magnus ◽  
Hubert H. Feucht ◽  
...  
Keyword(s):  
Immunoglobulin G ◽  
Staphylococcus Epidermidis ◽  
Biofilm Formation ◽  
Functional Role ◽  
Common Property ◽  
Polysaccharide Intercellular Adhesin ◽  
Functional Component ◽  
Negative Phenotype

ABSTRACT Hemagglutination of erythrocytes is a common property ofStaphylococcus epidermidis strains, which is related to adherence and biofilm formation and may be essential for the pathogenesis of biomaterial-associated infections caused byS. epidermidis. In three independent biofilm-producing, hemagglutination-positive S. epidermidis isolates, interruption of the icaADBC operon essential for polysaccharide intercellular adhesin (PIA) synthesis by Tn917 insertions led to a hemagglutination-negative phenotype. An immunoglobulin G fraction of antiserum to PIA greatly reduced hemagglutination. Purified PIA led to a 64-fold decrease of hemagglutination titers of these strains; however, it did not mediate hemagglutination by itself. These observations define PIA as the hemagglutinin of S. epidermidis or at least as its major functional component.

scholarly journals Inhibition of Staphylococcal Biofilm Formation by Nitrite

2007 ◽  
Vol 189 (21) ◽  
pp. 7911-7919 ◽  
Author(s):  
Steffen Schlag ◽  
Christiane Nerz ◽  
Timo A. Birkenstock ◽  
Florian Altenberend ◽  
Friedrich Götz
Keyword(s):  
Staphylococcus Epidermidis ◽  
Adaptive Response ◽  
Biofilm Formation ◽  
Iron Homeostasis ◽  
Nitrosative Stress ◽  
Transcriptional Analysis ◽  
Polysaccharide Intercellular Adhesin ◽  
Human Pathogens ◽  
Oxidative And Nitrosative Stress ◽  
Induced Stress

ABSTRACT Several environmental stresses have been demonstrated to increase polysaccharide intercellular adhesin (PIA) synthesis and biofilm formation by the human pathogens Staphylococcus aureus and Staphylococcus epidermidis. In this study we characterized an adaptive response of S. aureus SA113 to nitrite-induced stress and show that it involves concomitant impairment of PIA synthesis and biofilm formation. Transcriptional analysis provided evidence that nitrite, either as the endogenous product of respiratory nitrate reduction or after external addition, causes repression of the icaADBC gene cluster, mediated likely by IcaR. Comparative microarray analysis revealed a global change in gene expression during growth in the presence of 5 mM sodium nitrite and indicated a response to oxidative and nitrosative stress. Many nitrite-induced genes are involved in DNA repair, detoxification of reactive oxygen and nitrogen species, and iron homeostasis. Moreover, preformed biofilms could be eradicated by the addition of nitrite, likely the result of the formation of toxic acidified nitrite derivatives. Nitrite-mediated inhibition of S. aureus biofilm formation was abrogated by the addition of nitric oxide (NO) scavengers, suggesting that NO is directly or indirectly involved. Nitrite also repressed biofilm formation of S. epidermidis RP62A.

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