scholarly journals Inhibition ofStaphylococcus epidermidisBiofilm Formation by Traditional Thai Herbal Recipes Used for Wound Treatment

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
S. Chusri ◽  
K. Sompetch ◽  
S. Mukdee ◽  
S. Jansrisewangwong ◽  
T. Srichai ◽  
...  
Keyword(s):  
Staphylococcus Epidermidis ◽  
Biofilm Formation ◽  
Reference Strain ◽  
Ethanol Extract ◽  
Wound Treatment ◽  
Crystal Violet Staining ◽  
Reduction Assay ◽  
Mtt Reduction ◽  
Biofilm Development ◽  
Glass Surfaces

Development of biofilm is a key mechanism involved inStaphylococcus epidermidisvirulence during device-associated infections. We aimed to investigate antibiofilm formation and mature biofilm eradication ability of ethanol and water extracts of Thai traditional herbal recipes including THR-SK004, THR-SK010, and THR-SK011 againstS. epidermidis. A biofilm forming reference strain,S. epidermidisATCC 35984 was employed as a model for searching anti-biofilm agents by MTT reduction assay. The results revealed that the ethanol extract of THR-SK004 (THR-SK004E) could inhibit the formation ofS. epidermidisbiofilm on polystyrene surfaces. Furthermore, treatments with the extract efficiently inhibit the biofilm formation of the pathogen on glass surfaces determined by scanning electron microscopy and crystal violet staining. In addition, THR-SK010 ethanol extract (THR-SK010E; 0.63–5 μg/mL) could decrease 30 to 40% of the biofilm development. Almost 90% of a 7-day-old staphylococcal biofilm was destroyed after treatment with THR-SK004E (250 and 500 μg/mL) and THR-SK010E (10 and 20 μg/mL) for 24 h. Therefore, our results clearly demonstrated THR-SK004E could prevent the staphylococcal biofilm development, whereas both THR-SK004E and THR-SK010E possessed remarkable eradication ability on the mature staphylococcal biofilm.

scholarly journals Green Tea Polyphenols and Padma Hepaten Inhibit Candida albicans Biofilm Formation

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Yosi Farkash ◽  
Mark Feldman ◽  
Isaac Ginsburg ◽  
Doron Steinberg ◽  
Miriam Shalish
Keyword(s):  
Candida Albicans ◽  
Green Tea ◽  
Crystal Violet ◽  
Biofilm Formation ◽  
Host Cells ◽  
Green Tea Polyphenols ◽  
Crystal Violet Staining ◽  
Biofilm Inhibition ◽  
Therapeutic Concept ◽  
Biofilm Development

Candida albicans (C. albicans) is the most prevalent opportunistic human pathogenic fungus and can cause mucosal membrane infections and invade the blood. In the oral cavity, it can ferment dietary sugars, produce organic acids and therefore has a role in caries development. In this study, we examined whether the polyphenol rich extractions Polyphenon from green tea (PPFGT) and Padma Hepaten (PH) can inhibit the caries-inducing properties of C. albicans. Biofilms of C. albicans were grown in the presence of PPFGT and PH. Formation of biofilms was tested spectrophotometrically after crystal violet staining. Exopolysaccharides (EPS) secretion was quantified using confocal scanning laser microscopy (CSLM). Treated C. albicans morphology was demonstrated using scanning electron microscopy (SEM). Expression of virulence-related genes was tested using qRT-PCR. Development of biofilm was also tested on an orthodontic surface (Essix) to assess biofilm inhibition ability on such appliances. Both PPFGT and PH dose-dependently inhibited biofilm formation, with no inhibition on planktonic growth. The strongest inhibition was obtained using the combination of the substances. Crystal violet staining showed a significant reduction of 45% in biofilm formation using a concentration of 2.5mg/ml PPFGT and 0.16mg/ml PH. A concentration of 1.25 mg/ml PPFGT and 0.16 mg/ml PH inhibited candidal growth by 88% and EPS secretion by 74% according to CSLM. A reduction in biofilm formation and in the transition from yeast to hyphal morphotype was observed using SEM. A strong reduction was found in the expression of hwp1, eap1, and als3 virulence associated genes. These results demonstrate the inhibitory effect of natural PPFGT polyphenolic extraction on C. albicans biofilm formation and EPS secretion, alone and together with PH. In an era of increased drug resistance, the use of phytomedicine to constrain biofilm development, without killing host cells, may pave the way to a novel therapeutic concept, especially in children as orthodontic patients.

scholarly journals Improvement of XTT assay performance for studies involving Candida albicans biofilms

2008 ◽  
Vol 19 (4) ◽  
pp. 364-369 ◽  
Author(s):  
Wander José da Silva ◽  
Jayampath Seneviratne ◽  
Nipuna Parahitiyawa ◽  
Edvaldo Antonio Ribeiro Rosa ◽  
Lakshman Perera Samaranayake ◽  
...  
Keyword(s):  
Candida Albicans ◽  
Biofilm Formation ◽  
Cell Activity ◽  
Growth Yield ◽  
Xtt Assay ◽  
Biofilm Growth ◽  
Assay Performance ◽  
Reduction Assay ◽  
Cell Layers ◽  
Biofilm Development

2, 3-bis (2-methoxy-4-nitro-5-sulfophenyl)-5-[(phenylamino) carbonyl]-2H-tetrazolium hydroxide (XTT) reduction assay has been used to study Candida biofilm formation. However, considering that the XTT reduction assay is dependent on cell activity, its use for evaluating mature biofilms may lead to inaccuracies since biofilm bottom cell layers tend to be relatively quiescent at later stages of biofilm formation. The aim of this study was to improve XTT reduction assay by adding glucose supplements to the standard XTT formulation. Candida albicans ATCC 90028 was used to form 24-, 48- and 72-h biofilms. The oxidative activity at 90, 180 and 270 min of incubation was evaluated. The control consisted of standard XTT formulation without glucose supplements, and was modified by the addition of 50, 100 and 200 mM of glucose. The XTT assay with 200 mM glucose showed more accurate and consistent readings correlating with biofilm development at 24, 48 and 72 h. Biofilm growth yield after 180 min incubation, when evaluated with the 200 mM glucose supplemented XTT, produced the most consistent readings on repetitive testing. It may be concluded that glucose supplementation of XTT could minimize variation and produce more accurate data for the XTT assay.

scholarly journals Aryl Rhodanines Specifically Inhibit Staphylococcal and Enterococcal Biofilm Formation

2009 ◽  
Vol 53 (10) ◽  
pp. 4357-4367 ◽  
Author(s):  
Timothy J. Opperman ◽  
Steven M. Kwasny ◽  
John D. Williams ◽  
Atiyya R. Khan ◽  
Norton P. Peet ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Small Molecules ◽  
Staphylococcus Epidermidis ◽  
Biofilm Formation ◽  
Antibiofilm Activity ◽  
Bacterial Strains ◽  
Gram Negative ◽  
Artificial Surfaces ◽  
Causative Agents ◽  
Biofilm Development

ABSTRACT Staphylococcus epidermidis and Staphylococcus aureus are the leading causative agents of indwelling medical device infections because of their ability to form biofilms on artificial surfaces. Here we describe the antibiofilm activity of a class of small molecules, the aryl rhodanines, which specifically inhibit biofilm formation of S. aureus, S. epidermidis, Enterococcus faecalis, E. faecium, and E. gallinarum but not the gram-negative species Pseudomonas aeruginosa or Escherichia coli. The aryl rhodanines do not exhibit antibacterial activity against any of the bacterial strains tested and are not cytotoxic against HeLa cells. Preliminary mechanism-of-action studies revealed that the aryl rhodanines specifically inhibit the early stages of biofilm development by preventing attachment of the bacteria to surfaces.

scholarly journals Role of the luxS Quorum-Sensing System in Biofilm Formation and Virulence of Staphylococcus epidermidis

2006 ◽  
Vol 74 (1) ◽  
pp. 488-496 ◽  
Author(s):  
Lin Xu ◽  
Hualin Li ◽  
Cuong Vuong ◽  
Viveka Vadyvaloo ◽  
Jianping Wang ◽  
...  
Keyword(s):  
Quorum Sensing ◽  
Mutant Strain ◽  
Staphylococcus Epidermidis ◽  
Biofilm Formation ◽  
Bacterial Pathogens ◽  
Sensing System ◽  
Autoinducer 2 ◽  
Enhanced Production ◽  
Quorum Sensing System ◽  
Biofilm Development

ABSTRACT Nosocomial infections caused by Staphylococcus epidermidis are characterized by biofilm formation on implanted medical devices. Quorum-sensing regulation plays a major role in the biofilm development of many bacterial pathogens. Here, we describe luxS, a quorum-sensing system in staphylococci that has a significant impact on biofilm development and virulence. We constructed an isogenic ΔluxS mutant strain of a biofilm-forming clinical isolate of S. epidermidis and demonstrated that luxS signaling is functional in S. epidermidis. The mutant strain showed increased biofilm formation in vitro and enhanced virulence in a rat model of biofilm-associated infection. Genetic complementation and addition of autoinducer 2-containing culture filtrate restored the wild-type phenotype, demonstrating that luxS repressed biofilm formation through a cell-cell signaling mechanism based on autoinducer 2 secretion. Enhanced production of the biofilm exopolysaccharide polysaccharide intercellular adhesin in the mutant strain is presumably the major cause of the observed phenotype. The agr quorum-sensing system has previously been shown to impact biofilm development and biofilm-associated infection in a way similar to that of luxS, although by regulation of different factors. Our study indicates a general scheme of quorum-sensing regulation of biofilm development in staphylococci, which contrasts with that observed in many other bacterial pathogens.

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

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.

scholarly journals Vitamin E for prevention of biofilm-caused Healthcare-associated infections

Open Medicine ◽  
2019 ◽  
Vol 15 (1) ◽  
pp. 14-21 ◽  
Author(s):  
Franca Vergalito ◽  
Laura Pietrangelo ◽  
Giulio Petronio Petronio ◽  
Federica Colitto ◽  
Marco Alfio Cutuli ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Vitamin E ◽  
Staphylococcus Epidermidis ◽  
Biofilm Formation ◽  
Bacterial Colonization ◽  
Bacterial Biofilm ◽  
Tocopheryl Acetate ◽  
Healthcare Associated Infections ◽  
Biofilm Development ◽  
Healthcare Associated

AbstractThe healthcare-associated infections (HCAIs) occur in patients both in nosocomial environments and in community. More often HCAIs are associated to the use of medical devices and bacterial biofilm development on these equipments. Due to the clinical and economic relevance of this topic, new strategies for the treatment of infections caused by biofilm proliferation are unceasingly searched by scientists.The present study investigated the role of vitamin E to reduce the biofilm formation for a larger panel of human pathogens, including strains of Staphylococcus aureus, Staphylococcus epidermidis, Escherichia coli, Klebsiella pneumoniae, Proteus mirabilis, Acinetobacter baumannii, Pseudomonas aeruginosa and Pseudomonas putida.This potential activity was tested by placing a preparation of vitamin E (α-Tocopheryl acetate) as interface between the bacterial culture and the polystyrene walls of a 96 well plate at different concentrations of glucose, used as a biofilm enhancer.The Staphylococcus genus was further investigated by spreading the vitamin E on a silicone catheter lumen and evaluating its influence on the bacterial colonization.From our results, vitamin E has been able to interfere with bacterial biofilm and prevent in vitro biofilm formation. Furthermore, the ability of Staphylococcus aureus and Staphylococcus epidermidis to colonize the catheter surface decreased as a result of vitamin E application.

scholarly journals SarA Is an Essential Positive Regulator of Staphylococcus epidermidis Biofilm Development

2005 ◽  
Vol 187 (7) ◽  
pp. 2348-2356 ◽  
Author(s):  
María Ángeles Tormo ◽  
Miguel Martí ◽  
Jaione Valle ◽  
Adhar C. Manna ◽  
Ambrose L. Cheung ◽  
...  
Keyword(s):  
Virulence Factors ◽  
Staphylococcus Epidermidis ◽  
Biofilm Formation ◽  
Regulatory Element ◽  
Mobility Shift ◽  
Independent Manner ◽  
Positive Regulator ◽  
Reverse Transcription Pcr ◽  
O 47 ◽  
Biofilm Development

ABSTRACT Staphylococcus epidermidis biofilm formation is associated with the production of the polysaccharide intercellular adhesin (PIA)--poly-N-acetylglucosamine polysaccharide (PNAG) by the products of the icaADBC operon. Recent evidence indicates that SarA, a central regulatory element that controls the production of Staphylococcus aureus virulence factors, is essential for the synthesis of PIA/PNAG and the ensuing biofilm development in this species. Based on the presence of a sarA homolog, we hypothesized that SarA could also be involved in the regulation of the biofilm formation process in S. epidermidis. To investigate this, we constructed nonpolar sarA deletions in two genetically unrelated S. epidermidis clinical strains, O-47 and CH845. The SarA mutants were completely defective in biofilm formation, both in the steady-state conditions of a microtiter dish assay and in the flow conditions of microfermentors. Reverse transcription-PCR experiments showed that the mutation in the sarA gene resulted in downregulation of the icaADBC operon transcription in an IcaR-independent manner. Purified SarA protein showed high-affinity binding to the icaA promoter region by electrophoretic mobility shift assays. Consequently, mutation in sarA provoked a significant decrease in the amount of PIA/PNAG on the cell surface. Furthermore, heterologous complementation of S. aureus sarA mutants with the sarA gene of S. epidermidis completely restored biofilm formation. In summary, SarA appeared to be a positive regulator of transcription of the ica locus, and in its absence, PIA/PNAG production and biofilm formation were diminished. Additionally, we present experimental evidence showing that SarA may be an important regulatory element that controls S. epidermidis virulence factors other than biofilm formation.

scholarly journals ygsIs a Novel Gene That Influences Biofilm Formation and the General Stress Response ofStaphylococcus epidermidis

2010 ◽  
Vol 79 (3) ◽  
pp. 1007-1015 ◽  
Author(s):  
Xing Wang ◽  
Chen Niu ◽  
Gang Sun ◽  
Dandan Dong ◽  
Amer E. Villaruz ◽  
...  
Keyword(s):  
Stress Response ◽  
Staphylococcus Epidermidis ◽  
Biofilm Formation ◽  
Gene Encoding ◽  
General Stress Response ◽  
General Stress ◽  
Infection Models ◽  
Implanted Medical Devices ◽  
Biofilm Development ◽  
Stress Response Gene

ABSTRACTInfections caused by the nosocomial pathogenStaphylococcus epidermidisfrequently develop on implanted medical devices and involve biofilm formation. Biofilms are surface-attached microbial communities that show increased resistance to drug treatment and mechanisms of innate host defense. In this study, a mutant library of the clinical isolateS. epidermidis1457 was constructed using mariner-based transposon mutagenesis. About a thousand mutants were screened, and 12 mutants were identified as significantly defective in biofilm formation. We focused on a mutant in which the transposon had inserted in a gene with unknown function,SERP0541, which is annotated as a gene encoding a GSP13-like general stress response protein. The gene was namedygs(encoding an unknowngeneralstress protein). Various stresses, including heat, pH, high osmolarity, and ethanol affected the survival of theygsmutant to a significantly higher degree than the wild-type strain and led to increased expression ofygs. Furthermore, synthesis of polysaccharide intercellular adhesin (PIA) and transcription of the PIA biosynthetic operon were significantly decreased in theygsmutant. These results are in accordance with the putative involvement ofygsin stress-response gene regulation and indicate thatygsinfluences biofilm development by controlling PIA-dependent biofilm accumulation. Moreover,ygshad a significant impact on the formation of biofilms and metastatic disease in two catheter-related rat infection models. Our study shows that theygsgene controlsS. epidermidisbiofilm accumulation and stress resistance, representing a key regulator of both structural and physiological biofilm characteristics with a significant impact on biofilm-associated infection.

scholarly journals Inhibition of Staphylococcus epidermidis Biofilm by Trimethylsilane Plasma Coating

2012 ◽  
Vol 56 (11) ◽  
pp. 5923-5937 ◽  
Author(s):  
Yibao Ma ◽  
Meng Chen ◽  
John E. Jones ◽  
Andrew C. Ritts ◽  
Qingsong Yu ◽  
...  
Keyword(s):  
Antibiotic Treatment ◽  
Medical Devices ◽  
Staphylococcus Epidermidis ◽  
Biofilm Formation ◽  
Plasma Coating ◽  
Bacterial Cells ◽  
Implantable Medical Devices ◽  
Content Type ◽  
Coated Surfaces ◽  
Biofilm Development

ABSTRACTBiofilm formation on implantable medical devices is a major impediment to the treatment of nosocomial infections and promotes local progressive tissue destruction.Staphylococcus epidermidisinfections are the leading cause of biofilm formation on indwelling devices. Bacteria in biofilms are highly resistant to antibiotic treatment, which in combination with the increasing prevalence of antibiotic resistance among human pathogens further complicates treatment of biofilm-related device infections. We have developed a novel plasma coating technology. Trimethylsilane (TMS) was used as a monomer to coat the surfaces of 316L stainless steel and grade 5 titanium alloy, which are widely used in implantable medical devices. The results of biofilm assays demonstrated that this TMS coating markedly decreasedS. epidermidisbiofilm formation by inhibiting the attachment of bacterial cells to the TMS-coated surfaces during the early phase of biofilm development. We also discovered that bacterial cells on the TMS-coated surfaces were more susceptible to antibiotic treatment than their counterparts in biofilms on uncoated surfaces. These findings suggested that TMS coating could result in a surface that is resistant to biofilm development and also in a bacterial community that is more sensitive to antibiotic therapy than typical biofilms.

scholarly journals icaR Encodes a Transcriptional Repressor Involved in Environmental Regulation of ica Operon Expression and Biofilm Formation in Staphylococcus epidermidis

2002 ◽  
Vol 184 (16) ◽  
pp. 4400-4408 ◽  
Author(s):  
Kevin M. Conlon ◽  
Hilary Humphreys ◽  
James P. O'Gara
Keyword(s):  
Environmental Regulation ◽  
Staphylococcus Epidermidis ◽  
Biofilm Formation ◽  
Reference Strain ◽  
Fold Increase ◽  
Insertion Mutation ◽  
Phase Variable ◽  
Reversible Inactivation ◽  
Operon Expression ◽  
Phase Variants

ABSTRACT Biofilm formation in Staphylococcus epidermidis is dependent upon the ica operon-encoded polysaccharide intercellular adhesin, which is subject to phase-variable and environmental regulation. The icaR gene, located adjacent to the ica operon, appears to be a member of the tetR family of transcriptional regulators. In the reference strain RP62A, reversible inactivation of the ica operon by IS256 accounts for 25 to 33% of phase variants. In this study, icaA and icaR regulation were compared in RP62A and a biofilm-forming clinical isolate, CSF41498, in which IS256 is absent. Predictably, ica operon expression was detected only in wild-type CSF41498 and RP62A but not in non-IS256-generated phase variants. In contrast, the icaR gene was not expressed in RP62A phase variants but was expressed in CSF41498 variants. An icaR::Emr insertion mutation in CSF41498 resulted in an at least a 5.8-fold increase in ica operon expression but did not significantly alter regulation of the icaR gene itself. Activation of ica operon transcription by ethanol in CSF41498 was icaR dependent. In contrast, a small but significant induction of ica by NaCl and glucose (NaCl-glucose) was observed in the icaR::Emr mutant. In addition, transcription of the icaR gene itself was not significantly affected by NaCl-glucose but was repressed by ethanol. Expression of the ica operon was induced by ethanol or NaCl-glucose in phase variants of CSF41498 (icaR +) but not in RP62A variants (icaR deficient). These data indicate that icaR encodes a repressor of ica operon transcription required for ethanol but not NaCl-glucose activation of ica operon expression and biofilm formation.

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