scholarly journals Deletion of SarX decreases biofilm formation of Staphylococcus aureus in a polysaccharide intercellular adhesin (PIA) dependent manner

2020 ◽  
Author(s):  
Zhihao Hao ◽  
Yinjuan Guo ◽  
Lulin Rao ◽  
Jingyi Yu ◽  
Qing Zhan ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Mutant Strain ◽  
Biofilm Formation ◽  
Transcriptional Activity ◽  
Extracellular Proteins ◽  
Dependent Manner ◽  
Rt Pcr ◽  
Biofilm Production ◽  
Fold Reduction ◽  
Operon Expression

Abstract Background: Biofilm formation by Staphylococcus aureus is an important virulence determinant mediated by the polysaccharide intercellular adhere (PIA) encoded by ica operon or by surface and extracellular proteins. Previous studies have shown that S. epidermidis SarX protein regulated the transcriptional activity of the agr and ica loci and controled the biofilm phenotype, primarily by regulating icaADBC transcription and PIA production.Results: In this study, our results indicated that biofilm formation and detachment of S. aureus were significantly decreased in the sarX mutant strain. sarX mutant in S. aureus biofilm formation was related to the production of PIA and not to that of eDNA. RT-PCR results showed that deletion of sarX was associated with a 1.8-fold reduction in spa transcription, which was complemented by sarX. Expression of Spa protein was decreased in sarX mutant strain.Conclusions: sarX promoted biofilm production of S. aureus may mediated primarily through increasing ica operon expression and PIA production. Deletion of sarX was associated with reduction in spa transcription.

Identification of ica-dependent biofilm production by Staphylococcus aureus clinical isolates and antibiofilm effects of ascorbic acid against biofilm production

2020 ◽  
Vol 73 (5) ◽  
pp. 261-266
Author(s):  
Sahra Kırmusaoğlu ◽  
Havva Kaşıkçı
Keyword(s):  
Staphylococcus Aureus ◽  
Ascorbic Acid ◽  
Biofilm Formation ◽  
Surface Proteins ◽  
Clinical Isolates ◽  
High Morbidity ◽  
Dependent Manner ◽  
Independent Manner ◽  
Biofilm Production ◽  
Life Threatening

AimsStaphylococcus aureus (S. aureus) is a life-threatening pathogen with high morbidity and mortality rates which causes nosocomial and community-acquired infections. Biofilm, considered to be a common virulence factor for pathogens, plays a significant role in recurrent and untreatable infections. Biofilm formation of S. aureus is mediated by synthesis of either poly-N-acetylglucosamine in an ica-dependent manner or surface proteins in an ica-independent manner. In some cases treatment is impossible and recurrent. In this study, ica-dependent biofilm-producing S. aureus isolates were detected and the anti-biofilm effect of ascorbic acid against biofilm formation of isolates was investigated.MethodsA total of 21 methicillin-sensitive S. aureus (MSSA) clinical isolates stored in our bacterial stock were used to detect ica-dependent biofilm-producing MSSA isolates. The anti-biofilm study was undertaken with three ica-dependent biofilm-producing isolates (MSSA2–4) and ATCC 29213 (MSSA1). Biofilms and the anti-biofilm effect of ascorbic acid were detected using the microtitre plate (MtP) method. 16S-rRNA, nuc, icaA and icaD genes and expression levels of icaA and icaD of isolates were detected by RT-PCR.ResultsThe minimum inhibitory concentrations (MICs) of ascorbic acid prevented biofilm formation of MSSA1 and MSSA3. Also, 1/2 MIC of ascorbic acid prevented biofilm formation of MSSA3. It was observed that biofilm formation decreased with increased concentration. There was no significant increase in ica gene expression of MSSA1 and MSSA2. Expression of icaA and icaD of MSSA3 decreased 13% and 38%, respectively. Expression of icaA in MSSA4 decreased 12%.ConclusionThe results of our study show that ascorbic acid can be used as an anti-biofilm agent to prevent biofilm formation of S. aureus and thus biofilm-related infections.

scholarly journals Molecular Investigation of Fibronectin-Binding Protein Genes and Capacity of Biofilm Production in Staphylococcus Aureus Isolated From Clinical Samples

2021 ◽  
Author(s):  
Hossein Jafari Soghondicolaei ◽  
Mohammad Ahanjan ◽  
Mehrdad Gholami ◽  
Bahman Mirzaei ◽  
Hamid Reza Goli
Keyword(s):  
Staphylococcus Aureus ◽  
Biofilm Formation ◽  
Colorimetric Assay ◽  
Binding Protein ◽  
Clinical Isolates ◽  
Diffusion Method ◽  
Clinical Samples ◽  
Biofilm Production ◽  
Fibronectin Binding Protein ◽  
Fibronectin Binding

Abstract Biofilm production increases Staphylococcus aureus resistance to antibiotics and also host defense mechanisms. The current study aims to evaluate the biofilm formation by S. aureus and to determine the prevalence of fibronectin-binding protein genes, also its correlation with drug resistance. In this study, 100 clinical isolates of S. aureus were collected. The antibiotic susceptibility pattern of the isolates was evaluated by the disk agar diffusion method. The ability of biofilm formation in the studied isolates was also determined by microplate colorimetric assay. Then, all isolates were screened by polymerase chain reaction for the fnbA and fnbB genes. Out of 100 clinical isolates of S. aureus, the highest and lowest antibiotic resistance rates were against penicillin (94%) and vancomycin (6%). Thirty-two cases were found to be multi-drug resistant (MDR) among the all strains. The ability of biofilm production was observed in 89% of the isolates. The PCR results showed that the prevalence of fnbA and fnbB genes were 91% and 17%, respectively. Moreover, 100% and 21.8% of the MDR strains harbored the fnbA and fnbB genes respectively. The ability to form biofilm in MDR isolates of S. aureus is more than non-MDR isolates, especially fnbA positive ones. As the bacteria in the biofilm are difficult to kill by antibiotics, attention to the removal or control of the biofilm production seems to be necessary.

An Alanine-Rich Peptide Attenuates Quorum Sensing-Regulated Virulence and Biofilm Formation in Staphylococcus aureus

2019 ◽  
Vol 102 (4) ◽  
pp. 1228-1234 ◽  
Author(s):  
Raid Al Akeel ◽  
Ayesha Mateen ◽  
Rabbani Syed
Keyword(s):  
Gene Expression ◽  
Staphylococcus Aureus ◽  
Quorum Sensing ◽  
Biofilm Formation ◽  
Bacterial Attachment ◽  
The Body ◽  
Dependent Manner ◽  
Virulence Determinants ◽  
Microarray Gene Expression ◽  
Concentration Dependent Manner

Abstract Background: Alanine-rich proteins/peptides (ARP), with bioactivity of up to 20 amino acid residues, can be observed by the body easily during gastrointestinal digestion. Objective: Populus trichocarpa extract’s capability to attenuate quorum sensing-regulated virulence and biofilm formation in Staphylococcus aureus is described. Methods: PT13, an ARP obtained from P. trichocarpa, was tested for its activity against S. aureus using the broth microdilution test; a crystal-violet biofilm assay was performed under a scanning electron microscope. The production of various virulence factors was estimated with PT13 treatment. Microarray gene expression profiling of PT13-treated S. aureus was conducted and compared with an untreated control. Exopolysaccharides (EPS) was estimated to observe the PT13 inhibition activity. Results: PT13 was antimicrobial toward S. aureus at different concentrations and showed a similar growth rate in the presence and absence of PT13 at concentrations ≤8 μg/mL. Biofilm production was interrupted even at low concentrations, and biofilm-related genes were down-regulated when exposed to PT13. The genes encoding cell adhesion and bacterial attachment protein were the major genes suppressed by PT13. In addition, hemolysins, clumping activity, and EPS production of S. aureus decreased after treatment in a concentration-dependent manner. Conclusions: A long-chain PT13 with effective actions that, even at low concentration levels, not only regulated the gene expression in the producer organism but also blocked the virulence gene expression in this Gram-positive human pathogen is described. Highlights: We identified a PT13 as a potential antivirulence agent that regulated production of bacterial virulence determinants (e.g., toxins, enzymes and biofilm), downwards and it may be a promising anti-virulence agent to be further developed as an anti-infective agent.

scholarly journals Protein A-Mediated Multicellular Behavior in Staphylococcus aureus

2008 ◽  
Vol 191 (3) ◽  
pp. 832-843 ◽  
Author(s):  
Nekane Merino ◽  
Alejandro Toledo-Arana ◽  
Marta Vergara-Irigaray ◽  
Jaione Valle ◽  
Cristina Solano ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Biofilm Formation ◽  
Protein A ◽  
Surface Proteins ◽  
Growth Media ◽  
Dependent Manner ◽  
Chronic Infections ◽  
The Matrix ◽  
Implanted Medical Devices ◽  
Biofilm Development

ABSTRACT The capacity of Staphylococcus aureus to form biofilms on host tissues and implanted medical devices is one of the major virulence traits underlying persistent and chronic infections. The matrix in which S. aureus cells are encased in a biofilm often consists of the polysaccharide intercellular adhesin (PIA) or poly-N-acetyl glucosamine (PNAG). However, surface proteins capable of promoting biofilm development in the absence of PIA/PNAG exopolysaccharide have been described. Here, we used two-dimensional nano-liquid chromatography and mass spectrometry to investigate the composition of a proteinaceous biofilm matrix and identified protein A (spa) as an essential component of the biofilm; protein A induced bacterial aggregation in liquid medium and biofilm formation under standing and flow conditions. Exogenous addition of synthetic protein A or supernatants containing secreted protein A to growth media induced biofilm development, indicating that protein A can promote biofilm development without being covalently anchored to the cell wall. Protein A-mediated biofilm formation was completely inhibited in a dose-dependent manner by addition of serum, purified immunoglobulin G, or anti-protein A-specific antibodies. A murine model of subcutaneous catheter infection unveiled a significant role for protein A in the development of biofilm-associated infections, as the amount of protein A-deficient bacteria recovered from the catheter was significantly lower than that of wild-type bacteria when both strains were used to coinfect the implanted medical device. Our results suggest a novel role for protein A complementary to its known capacity to interact with multiple immunologically important eukaryotic receptors.

scholarly journals PYED-1 Inhibits Biofilm Formation and Disrupts the Preformed Biofilm of Staphylococcus aureus

Antibiotics ◽  
2020 ◽  
Vol 9 (5) ◽  
pp. 240 ◽  
Author(s):  
Adriana Vollaro ◽  
Anna Esposito ◽  
Eliana Pia Esposito ◽  
Raffaele Zarrilli ◽  
Annalisa Guaragna ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Quorum Sensing ◽  
Biofilm Formation ◽  
Surface Proteins ◽  
Transcriptional Analysis ◽  
Capsular Polysaccharides ◽  
Dependent Manner ◽  
Chronic Infections ◽  
Concentration Dependent Manner ◽  
Expression Of Genes

Pregnadiene-11-hydroxy-16α,17α-epoxy-3,20-dione-1 (PYED-1), a heterocyclic corticosteroid derivative of deflazacort, exhibits broad-spectrum antibacterial activity against Gram-negative and Gram-positive bacteria. Here, we investigated the effect of PYED-1 on the biofilms of Staphylococcus aureus, an etiological agent of biofilm-based chronic infections such as osteomyelitis, indwelling medical device infections, periodontitis, chronic wound infections, and endocarditis. PYED-1 caused a strong reduction in biofilm formation in a concentration dependent manner. Furthermore, it was also able to completely remove the preformed biofilm. Transcriptional analysis performed on the established biofilm revealed that PYED-1 downregulates the expression of genes related to quorum sensing (agrA, RNAIII, hld, psm, and sarA), surface proteins (clfB and fnbB), secreted toxins (hla, hlb, and lukD), and capsular polysaccharides (capC). The expression of genes that encode two main global regulators, sigB and saeR, was also significantly inhibited after treatment with PYED-1. In conclusion, PYED-1 not only effectively inhibited biofilm formation, but also eradicated preformed biofilms of S. aureus, modulating the expression of genes related to quorum sensing, surface and secreted proteins, and capsular polysaccharides. These results indicated that PYED-1 may have great potential as an effective antibiofilm agent to prevent S. aureus biofilm-associated infections.

Deletion of mazF increases Staphylococcus aureus biofilm formation in an ica-dependent manner

2017 ◽  
Vol 75 (5) ◽  
Author(s):  
Fuminori Kato ◽  
Yusuke Yabuno ◽  
Yoshihiro Yamaguchi ◽  
Motoyuki Sugai ◽  
Masayori Inouye
Keyword(s):  
Staphylococcus Aureus ◽  
Biofilm Formation ◽  
Dependent Manner

scholarly journals The Active Component of Aspirin, Salicylic Acid, Promotes Staphylococcus aureus Biofilm Formation in a PIA-dependent Manner

2017 ◽  
Vol 8 ◽  
Author(s):  
Cristian Dotto ◽  
Andrea Lombarte Serrat ◽  
Natalia Cattelan ◽  
María S. Barbagelata ◽  
Osvaldo M. Yantorno ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Salicylic Acid ◽  
Biofilm Formation ◽  
Active Component ◽  
Dependent Manner

scholarly journals Deletion of SarX Decreases Biofilm Formation of Staphylococcus aureus in a Polysaccharide Intercellular Adhesin (PIA)-Dependent Manner by Downregulating spa

2021 ◽  
Vol Volume 14 ◽  
pp. 2241-2250
Author(s):  
Zhihao Hao ◽  
Yinjuan Guo ◽  
Lulin Rao ◽  
Jingyi Yu ◽  
Qing Zhan ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Biofilm Formation ◽  
Dependent Manner ◽  
Polysaccharide Intercellular Adhesin

Staphylococcus aureus: biofilm formation and strategies against it

2021 ◽  
Vol 22 ◽  
Author(s):  
Ahmad Nasser ◽  
Mohammad Mehdi Soltan Dallal ◽  
Shiva Jahanbakhshi ◽  
Taher Azimi ◽  
Leila Nikouei
Keyword(s):  
Staphylococcus Aureus ◽  
Drug Resistance ◽  
Quorum Sensing ◽  
Antimicrobial Therapy ◽  
Biofilm Formation ◽  
Bacterial Species ◽  
Influential Factors ◽  
Quorum Sensing Inhibitors ◽  
Biofilm Production ◽  
Biofilm Inhibitor

: The formation of Staphylococcus aureus biofilm causes significant infections in the human body. Biofilm forms through the aggregation of bacterial species and brings about many complications. It mediates drug resistance and persistence and facilitates the recurrence of infection at the end of antimicrobial therapy. Biofilm formation goes through a series of steps to complete, and any interference in these steps can disrupt its formation. Such interference may occur at any stage of biofilm production, including attachment, monolayer formation, and accumulation. Interfering agents can act as quorum sensing inhibitors and interfere in the functionality of quorum sensing receptors, attachment inhibitors and affect the cell hydrophobicity. Among these inhibiting strategies, attachment inhibitors could serve as the best agents against biofilm formation. If pathogens abort the attachment, the following stages of biofilm formation, e.g., accumulation and dispersion, will fail to materialize. Inhibition at this stage leads to suppression of virulence factors and invasion. One of the best-known inhibitors is a chelator that collects metal, Fe+, Zn+, and magnesium critical for biofilm formation. These influential factors in the binding and formation of biofilm are investigated, and the coping strategy is discussed. This review examines the stages of biofilm formation and determines what factors interfere in the continuity of these steps. Finally, the inhibition strategies are investigated, reviewed, and discussed. Keywords: Biofilm, Staphylococcus, Biofilm inhibitor, Dispersion, Antibiofilm agent, EPS, PIA.

Sign in / Sign up

Export Citation Format

Share Document