scholarly journals Eugenol-Functionalized Magnetite Nanoparticles Modulate Virulence and Persistence in Pseudomonas aeruginosa Clinical Strains

Molecules ◽  
2021 ◽  
Vol 26 (8) ◽  
pp. 2189
Author(s):  
Hamzah Basil Mohammed ◽  
Sajjad Mohsin I. Rayyif ◽  
Carmen Curutiu ◽  
Alexandra Catalina Birca ◽  
Ovidiu-Cristian Oprea ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Biofilm Formation ◽  
Spherical Shape ◽  
Infectious Process ◽  
Phenotypic Resistance ◽  
Persistent Infections ◽  
Resistant Mutants ◽  
Subinhibitory Concentrations ◽  
Pathogenic Agents ◽  
Soluble Enzymes

Efficient antibiotics to cure Pseudomonas aeruginosa persistent infections are currently insufficient and alternative options are needed. A promising lead is to design therapeutics able to modulate key phenotypes in microbial virulence and thus control the progression of the infectious process without selecting resistant mutants. In this study, we developed a nanostructured system based on Fe3O4 nanoparticles (NPs) and eugenol, a natural plant-compound which has been previously shown to interfere with microbial virulence when utilized in subinhibitory concentrations. The obtained functional NPs are crystalline, with a spherical shape and 10–15 nm in size. The subinhibitory concentrations (MIC 1/2) of the eugenol embedded magnetite NPs (Fe3O4@EUG) modulate key virulence phenotypes, such as attachment, biofilm formation, persister selection by ciprofloxacin, and the production of soluble enzymes. To our knowledge, this is the first report on the ability of functional magnetite NPs to modulate P. aeruginosa virulence and phenotypic resistance; our data highlights the potential of these bioactive nanostructures to be used as anti-pathogenic agents.

scholarly journals Subinhibitory concentrations of the cationic antimicrobial peptide colistin induce the pseudomonas quinolone signal in Pseudomonas aeruginosa

Microbiology ◽  
2009 ◽  
Vol 155 (9) ◽  
pp. 2826-2837 ◽  
Author(s):  
Joanne Cummins ◽  
F. Jerry Reen ◽  
Christine Baysse ◽  
Marlies J. Mooij ◽  
Fergal O'Gara
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Antimicrobial Peptide ◽  
Biofilm Formation ◽  
Bacterial Colonization ◽  
Central Component ◽  
Functional Genomic ◽  
Cationic Antimicrobial Peptide ◽  
Altered Expression ◽  
Pseudomonas Quinolone Signal ◽  
Subinhibitory Concentrations

Colistin is an important cationic antimicrobial peptide (CAMP) in the fight against Pseudomonas aeruginosa infection in cystic fibrosis (CF) lungs. The effects of subinhibitory concentrations of colistin on gene expression in P. aeruginosa were investigated by transcriptome and functional genomic approaches. Analysis revealed altered expression of 30 genes representing a variety of pathways associated with virulence and bacterial colonization in chronic infection. These included response to osmotic stress, motility, and biofilm formation, as well as genes associated with LPS modification and quorum sensing (QS). Most striking was the upregulation of Pseudomonas quinolone signal (PQS) biosynthesis genes, including pqsH, pqsB and pqsE, and the phenazine biosynthesis operon. Induction of this central component of the QS network following exposure to subinhibitory concentrations of colistin may represent a switch to a more robust population, with increased fitness in the competitive environment of the CF lung.

Glycerol metabolism promotes biofilm formation byPseudomonas aeruginosa

2016 ◽  
Vol 62 (8) ◽  
pp. 704-710 ◽  
Author(s):  
Jessica Scoffield ◽  
Laura Silo-Suh
Keyword(s):  
Cystic Fibrosis ◽  
Fatty Acids ◽  
Pseudomonas Aeruginosa ◽  
Host Cell ◽  
Biofilm Formation ◽  
Glycerol Metabolism ◽  
Persistent Infections ◽  
Expression Of Genes ◽  
Key Factor ◽  
Host Cell Membranes

Pseudomonas aeruginosa causes persistent infections in the airways of cystic fibrosis (CF) patients. Airway sputum contains various host-derived nutrients that can be utilized by P. aeruginosa, including phosphotidylcholine, a major component of host cell membranes. Phosphotidylcholine can be degraded by P. aeruginosa to glycerol and fatty acids to increase the availability of glycerol in the CF lung. In this study, we explored the role that glycerol metabolism plays in biofilm formation by P. aeruginosa. We report that glycerol metabolism promotes biofilm formation by both a chronic CF isolate (FRD1) and a wound isolate (PAO1) of P. aeruginosa. Moreover, loss of the GlpR regulator, which represses the expression of genes involved in glycerol metabolism, enhances biofilm formation in FRD1 through the upregulation of Pel polysaccharide. Taken together, our results suggest that glycerol metabolism may be a key factor that contributes to P. aeruginosa persistence by promoting biofilm formation.

scholarly journals In vitro activities of cellulase and ceftazidime, alone and in combination against Pseudomonas aeruginosa biofilms

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Esmat Kamali ◽  
Ailar Jamali ◽  
Ahdieh Izanloo ◽  
Abdollah Ardebili
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Antibiotic Resistance ◽  
Biofilm Formation ◽  
Glycoside Hydrolase ◽  
Dependent Manner ◽  
Wound Infections ◽  
Persistent Infections ◽  
Novel Strategy ◽  
Dose Dependent

Abstract Background Biofilms are a main pathogenicity feature of Pseudomonas aeruginosa and has a significant role in antibiotic resistance and persistent infections in humans. We investigated the in vitro activities of antibiotic ceftazidime and enzyme cellulase, either alone or in combination against biofilms of P. aeruginosa. Results Both ceftazidime and cellulase significantly decreased biofilm formation in all strains in a dose-dependent manner. Combination of enzyme at concentrations of 1.25, 2.5, 5, and 10 U/mL tested with 1/16× MIC of antibiotic led to a significant reduction in biofilm biomass. Cellulase showed a significant detachment effect on biofilms at three concentrations of 10 U/mL, 5 U/mL, and 2.5 U/mL. The MIC, MBC, and MBEC values of ceftazidime were 2 to 4 µg/mL, 4 to 8 µg/mL, and 2048 to 8192 µg/mL. When combined with cellulase, the MBECs of antibiotic showed a significant decrease from 32- to 128-fold. Conclusions Combination of the ceftazidime and the cellulase had significant anti-biofilm effects, including inhibition of biofilm formation and biofilm eradication in P. aeruginosa. These data suggest that glycoside hydrolase therapy as a novel strategy has the potential to enhance the efficacy of antibiotics and helps to resolve biofilm-associated wound infections caused by this pathogen.

scholarly journals Pseudomonas aeruginosa Biofilm Formation and Its Control

Biologics ◽  
2021 ◽  
Vol 1 (3) ◽  
pp. 312-336
Author(s):  
Aishwarya Vetrivel ◽  
Monica Ramasamy ◽  
Preethi Vetrivel ◽  
Santhi Natchimuthu ◽  
Shobana Arunachalam ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Biofilm Formation ◽  
Treatment Options ◽  
Treatment Strategies ◽  
Natural Resistance ◽  
Causative Organism ◽  
Chronic Infections ◽  
Persistent Infections ◽  
Inappropriate Treatment ◽  
Conventional Antibiotics

Microbes are hardly seen as planktonic species and are most commonly found as biofilm communities in cases of chronic infections. Biofilms are regarded as a biological condition, where a large group of microorganisms gets adhered to a biotic or abiotic surface. In this context, Pseudomonas aeruginosa, a Gram-negative nosocomial pathogen is the main causative organism responsible for life-threatening and persistent infections in individuals affected with cystic fibrosis and other lung ailments. The bacteria can form a strong biofilm structure when it adheres to a surface suitable for the development of a biofilm matrix. These bacterial biofilms pose higher natural resistance to conventional antibiotic therapy due to their multiple tolerance mechanisms. This prevailing condition has led to an increasing rate of treatment failures associated with P. aeruginosa biofilm infections. A better understanding of the effect of a diverse group of antibiotics on established biofilms would be necessary to avoid inappropriate treatment strategies. Hence, the search for other alternative strategies as effective biofilm treatment options has become a growing area of research. The current review aims to give an overview of the mechanisms governing biofilm formation and the different strategies employed so far in the control of biofilm infections caused by P. aeruginosa. Moreover, this review can also help researchers to search for new antibiofilm agents to tackle the effect of biofilm infections that are currently imprudent to conventional antibiotics.

scholarly journals Quantitative mapping of mRNA 3’ ends in Pseudomonas aeruginosa reveals a pervasive role for premature 3’ end formation in response to azithromycin

PLoS Genetics ◽  
2021 ◽  
Vol 17 (7) ◽  
pp. e1009634
Author(s):  
Salini Konikkat ◽  
Michelle R. Scribner ◽  
Rory Eutsey ◽  
N. Luisa Hiller ◽  
Vaughn S. Cooper ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Pseudomonas Aeruginosa ◽  
Biofilm Formation ◽  
Molecular Mechanisms ◽  
Transcriptional Response ◽  
Cost Effective ◽  
Chronic Infections ◽  
Biofilm Growth ◽  
Persistent Infections ◽  
Transcriptional Pausing

Pseudomonas aeruginosa produces serious chronic infections in hospitalized patients and immunocompromised individuals, including patients with cystic fibrosis. The molecular mechanisms by which P. aeruginosa responds to antibiotics and other stresses to promote persistent infections may provide new avenues for therapeutic intervention. Azithromycin (AZM), an antibiotic frequently used in cystic fibrosis treatment, is thought to improve clinical outcomes through a number of mechanisms including impaired biofilm growth and quorum sensing (QS). The mechanisms underlying the transcriptional response to AZM remain unclear. Here, we interrogated the P. aeruginosa transcriptional response to AZM using a fast, cost-effective genome-wide approach to quantitate RNA 3’ ends (3pMap). We also identified hundreds of P. aeruginosa genes with high incidence of premature 3’ end formation indicative of riboregulation in their transcript leaders using 3pMap. AZM treatment of planktonic and biofilm cultures alters the expression of hundreds of genes, including those involved in QS, biofilm formation, and virulence. Strikingly, most genes downregulated by AZM in biofilms had increased levels of intragenic 3’ ends indicating premature transcription termination, transcriptional pausing, or accumulation of stable intermediates resulting from the action of nucleases. Reciprocally, AZM reduced premature intragenic 3’ end termini in many upregulated genes. Most notably, reduced termination accompanied robust induction of obgE, a GTPase involved in persister formation in P. aeruginosa. Our results support a model in which AZM-induced changes in 3’ end formation alter the expression of central regulators which in turn impairs the expression of QS, biofilm formation and stress response genes, while upregulating genes associated with persistence.

scholarly journals Enhancement of pyocyanin production by subinhibitory concentration of royal jelly in Pseudomonas aeruginosa

F1000Research ◽  
2021 ◽  
Vol 10 ◽  
pp. 14
Author(s):  
Dina Auliya Amly ◽  
Puspita Hajardhini ◽  
Alma Linggar Jonarta ◽  
Heribertus Dedy Kusuma Yulianto ◽  
Heni Susilowati
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Bacterial Growth ◽  
Biofilm Formation ◽  
Royal Jelly ◽  
Microtiter Plate ◽  
Clinical Isolates ◽  
Antibiotic Tolerance ◽  
Subinhibitory Concentration ◽  
Subinhibitory Concentrations ◽  
Pyocyanin Production

Background: Pseudomonas aeruginosa, a multidrug-resistant Gram-negative bacterium, produces pyocyanin, a virulence factor associated with antibiotic tolerance. High concentrations of royal jelly have an antibacterial effect, which may potentially overcome antibacterial resistance. However, in some cases, antibiotic tolerance can occur due to prolonged stress of low-dose antibacterial agents. This study aimed to investigate the effect of subinhibitory concentrations of royal jelly on bacterial growth, pyocyanin production, and biofilm formation of P. aeruginosa. Methods: Pseudomonas aeruginosa ATCC 10145 and clinical isolates were cultured in a royal jelly-containing medium to test the antibacterial activity. Pyocyanin production was observed by measuring the absorbance at 690 nm after 36 h culture and determined using extinction coefficient 4310 M-1 cm-1. Static microtiter plate biofilm assay performed to detect the biofilm formation, followed by scanning electron microscopy. Results: Royal jelly effectively inhibited the viability of both strains from a concentration of 25%. The highest production of pyocyanin was observed in the subinhibitory concentration group 6.25%, which gradually decreased along with the decrease of royal jelly concentration. Results of one-way ANOVA tests differed significantly in pyocyanin production of the two strains between the royal jelly groups. Tukey HSD test showed concentrations of 12.5%, 6.25%, and 3.125% significantly increased pyocyanin production of ATCC 10145, and the concentrations of 12.5% and 6.25% significantly increased production of the clinical isolates. Concentrations of 12.5% and 6.125% significantly induced biofilm formation of P. aeruginosa ATCC 10145, in line with the results of the SEM analysis. Conclusions: Royal jelly concentrations of 25% or higher can inhibit bacterial growth; however, subinhibitory concentrations could increase pyocyanin production and biofilm formation in P. aeruginosa. It is advisable to determine the appropriate concentration of royal jelly to obtain beneficial virulence inhibiting activity.

Better treatment options through a better understanding of Pseudomonas aeruginosa biofilm formation and biofilm-mediated resistance

2020 ◽  
Author(s):  
Jules Valentin ◽  
Adithi R. Varadarajan ◽  
Christian H. Ahrens ◽  
Henny van der Mei ◽  
Qun Ren
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Biofilm Formation ◽  
Response Regulator ◽  
Treatment Options ◽  
Underlying Mechanism ◽  
Chronic Infections ◽  
Persistent Infections ◽  
Planktonic Bacteria ◽  
Airway Infections ◽  
The Impact

<p>Bacteria living in biofilms tolerate much higher antibiotic concentrations compared to planktonic bacteria and can cause chronic infections. Among the most difficult pathogens to treat, <em>Pseudomonas aeruginosa</em> is responsible for many biofilm-related infections and for much of the mortality associated with airway infections in cystic fibrosis. We speculated that there are specific genes responsible for increased antibiotic resistance in biofilms and aimed to identify them in <em>P. aeruginosa</em>. By doing so, a better understanding of biofilm-mediated resistance can be achieved and new bacterial targets can be identified. A <em>P. aeruginosa</em> transposon mutant library was screened to assess the impact on biofilm formation and the biofilm resistance toward antibiotics. Briefly, the biofilm resistance was estimated by following the re-growth of biofilm cells exposed to different concentrations of antibiotics. A few candidates, e. g. the response regulator CbrB, involved in nutrient uptake, have been identified as crucial for biofilm formation and resistance towards antibiotics. Further characterization of these interesting genes has been carried out to explore the underlying mechanism of resistance. Such knowledge can lead to the identification of susceptibility of <em>P. aeruginosa</em> biofilm and help to develop tools to treat persistent infections.</p>

Bioactivity of Phenolic Compounds Extracted from Strawberry against Formation of Pseudomonas aeruginosa Biofilm

2019 ◽  
Vol 10 (01) ◽  
Author(s):  
Baydaa Hussein ◽  
Zainab A. Aldhaher ◽  
Shahrazad Najem Abdu-Allah ◽  
Adel Hamdan
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Phenolic Compounds ◽  
Biofilm Formation ◽  
Opportunistic Infections ◽  
Formation Rate ◽  
Hydrocarbon Chain ◽  
Health Concern ◽  
Gas Chromatography Mass Spectrometry ◽  
Phenolic Contents

Background: Biofilm is a bacterial way of life prevalent in the world of microbes; in addition to that it is a source of alarm in the field of health concern. Pseudomonas aeruginosa is a pathogenic bacterium responsible for all opportunistic infections such as chronic and severe. Aim of this study: This paper aims to provide an overview of the promotion of isolates to produce a biofilm in vitro under special circumstances, to expose certain antibiotics to produce phenotypic evaluation of biofilm bacteria. Methods and Materials: Three diverse ways were used to inhibited biofilm formation of P.aeruginosa by effect of phenolic compounds extracts from strawberries. Isolates produced biofilm on agar MacConkey under certain circumstances. Results: The results showed that all isolates were resistant to antibiotics except sensitive to azithromycin (AZM, 15μg), and in this study was conducted on three ways to detect the biofilm produced, has been detected by the biofilm like Tissue culture plate (TCP), Tube method (TM), Congo Red Agar (CRA). These methods gave a clear result of these isolates under study. Active compounds were analyzed in both extracts by Gas Chromatography-mass Spectrometry which indicate High molecular weight compound with a long hydrocarbon chain. Conclusion: Phenolic compounds could behave as bioactive material and can be useful to be used in pharmaceutical synthesis. Phenolic contents which found in leaves and fruits extracts of strawberries shows antibacterial activity against all strains tested by the ability to reduce the production of biofilm formation rate.

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