scholarly journals A Potential Quorum-Sensing Inhibitor for Bronchiectasis Therapy: Quercetin–Chitosan Nanoparticle Complex Exhibiting Superior Inhibition of Biofilm Formation and Swimming Motility of Pseudomonas aeruginosa to the Native Quercetin

2021 ◽  
Vol 22 (4) ◽  
pp. 1541
Author(s):  
The-Thien Tran ◽  
Kunn Hadinoto
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Quorum Sensing ◽  
Biofilm Formation ◽  
Bacterial Pathogen ◽  
Preparation Condition ◽  
Anticancer Activities ◽  
Swimming Motility ◽  
Amorphous Nanoparticle ◽  
Kinetic Solubility ◽  
Nanoparticle Complex

Quercetin (QUE)—a plant-derived flavonoid, is recently established as an effective quorum sensing (QS) inhibiting agent in Pseudomonas aeruginosa—the main bacterial pathogen in bronchiectasis lungs. Successful clinical application of QUE, however, is hindered by its low solubility in physiological fluids. Herein we developed a solubility enhancement strategy of QUE in the form of a stable amorphous nanoparticle complex (nanoplex) of QUE and chitosan (CHI), which was prepared by electrostatically driven complexation between ionized QUE molecules and oppositely charged CHI. At its optimal preparation condition, the QUE–CHI nanoplex exhibited a size of roughly 150 nm with a 25% QUE payload and 60% complexation efficiency. The complexation with CHI had no adverse effect on the antibacterial and anticancer activities of QUE, signifying the preservation of QUE’s bioactivities in the nanoplex. Compared to the native QUE, the QUE–CHI nanoplex exhibited superior QS inhibition in suppressing the QS-regulated swimming motility and biofilm formation of P. aeruginosa, but not in suppressing the virulence factor production. The superior inhibitions of the biofilm formation and swimming motility afforded by the nanoplex were attributed to (1) its higher kinetic solubility (5-times higher) that led to higher QUE exposures, and (2) the synergistic QS inhibition attributed to its CHI fraction.

Inhibition of biofilm formation and quorum sensing mediated virulence in Pseudomonas aeruginosa by marine sponge symbiont Brevibacterium casei strain Alu 1

2021 ◽  
Vol 150 ◽  
pp. 104693
Author(s):  
Nagasundaram Rashiya ◽  
Nagarajan Padmini ◽  
Antony Alex Kennedy Ajilda ◽  
Pandiyan Prabakaran ◽  
Ravindran Durgadevi ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Quorum Sensing ◽  
Marine Sponge ◽  
Biofilm Formation

scholarly journals Biofilm Formation in Pseudomonas aeruginosa: Fimbrial cup Gene Clusters Are Controlled by the Transcriptional Regulator MvaT

2004 ◽  
Vol 186 (9) ◽  
pp. 2880-2890 ◽  
Author(s):  
Isabelle Vallet ◽  
Stephen P. Diggle ◽  
Rachael E. Stacey ◽  
Miguel Cámara ◽  
Isabelle Ventre ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Biofilm Formation ◽  
Dna Microarrays ◽  
Transcriptional Profiling ◽  
Bacterial Pathogen ◽  
Gene Clusters ◽  
Northern Blotting ◽  
Negative Regulator ◽  
Regulatory Control ◽  
Homologous Gene

ABSTRACT Pseudomonas aeruginosa is an opportunistic bacterial pathogen which poses a major threat to long-term-hospitalized patients and individuals with cystic fibrosis. The capacity of P. aeruginosa to form biofilms is an important requirement for chronic colonization of human tissues and for persistence in implanted medical devices. Various stages of biofilm formation by this organism are mediated by extracellular appendages, such as type IV pili and flagella. Recently, we identified three P. aeruginosa gene clusters that were termed cup (chaperone-usher pathway) based on their sequence relatedness to the chaperone-usher fimbrial assembly pathway in other bacteria. The cupA gene cluster, but not the cupB or cupC cluster, is required for biofilm formation on abiotic surfaces. In this study, we identified a gene (mvaT) encoding a negative regulator of cupA expression. Such regulatory control was confirmed by several approaches, including lacZ transcriptional fusions, Northern blotting, and transcriptional profiling using DNA microarrays. MvaT also represses the expression of the cupB and cupC genes, although the extent of the regulatory effect is not as pronounced as with cupA. Consistent with this finding, mvaT mutants exhibit enhanced biofilm formation. Although the P. aeruginosa genome contains a highly homologous gene, mvaU, the repression of cupA genes is MvaT specific. Thus, MvaT appears to be an important regulatory component within a complex network that controls biofilm formation and maturation in P. aeruginosa.

Putrescine and its metabolic precursor arginine promote biofilm and c-di-GMP synthesis in Pseudomonas aeruginosa

2021 ◽  
Author(s):  
Zhexian Liu ◽  
Sarzana S. Hossain ◽  
Zayda Morales Moreira ◽  
Cara H. Haney
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Immune Responses ◽  
Biofilm Formation ◽  
Antimicrobial Agents ◽  
Bacterial Pathogen ◽  
Guanosine Monophosphate ◽  
Genetic Approach ◽  
Chronic Infections ◽  
Host Immune Responses ◽  
Primary Mechanism

Pseudomonas aeruginosa , an opportunistic bacterial pathogen can synthesize and catabolize a number of small cationic molecules known as polyamines. In several clades of bacteria polyamines regulate biofilm formation, a lifestyle-switching process that confers resistance to environmental stress. The polyamine putrescine and its biosynthetic precursors, L-arginine and agmatine, promote biofilm formation in Pseudomonas spp. However, it remains unclear whether the effect is a direct effect of polyamines or through a metabolic derivative. Here we used a genetic approach to demonstrate that putrescine accumulation, either through disruption of the spermidine biosynthesis pathway or the catabolic putrescine aminotransferase pathway, promoted biofilm formation in P. aeruginosa . Consistent with this observation, exogenous putrescine robustly induced biofilm formation in P. aeruginosa that was dependent on putrescine uptake and biosynthesis pathways. Additionally, we show that L-arginine, the biosynthetic precursor of putrescine, also promoted biofilm formation, but via a mechanism independent of putrescine or agmatine conversion. We found that both putrescine and L-arginine induced a significant increase in the intracellular level of bis-(3′-5′)-cyclic dimeric guanosine monophosphate (c-di-GMP) (c-di-GMP), a bacterial second messenger widely found in Proteobacteria that upregulates biofilm formation. Collectively these data show that putrescine and its metabolic precursor arginine promote biofilm and c-di-GMP synthesis in P. aeruginosa . Importance: Biofilm formation allows bacteria to physically attach to a surface, confers tolerance to antimicrobial agents, and promotes resistance to host immune responses. As a result, regulation of biofilm is often crucial for bacterial pathogens to establish chronic infections. A primary mechanism of biofilm promotion in bacteria is the molecule c-di-GMP, which promotes biofilm formation. The level of c-di-GMP is tightly regulated by bacterial enzymes. In this study, we found that putrescine, a small molecule ubiquitously found in eukaryotic cells, robustly enhances P. aeruginosa biofilm and c-di-GMP. We propose that P. aeruginosa may sense putrescine as a host-associated signal that triggers a lifestyle switching that favors chronic infection.

Inhibition of biofilm formation and quorum sensing by soy isoflavones in Pseudomonas aeruginosa

Food Control ◽  
2021 ◽  
pp. 108629
Author(s):  
Liqing Yin ◽  
Yongzhu Zhang ◽  
Fidelis Azi ◽  
Jianzhong Zhou ◽  
Xiaoli Liu ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Quorum Sensing ◽  
Biofilm Formation ◽  
Soy Isoflavones

scholarly journals Antimicrobial Resistance and Biofilm Formation of Pseudomonas aeruginosa

10.3823/846 ◽  
2020 ◽  
Vol 10 (2) ◽  
Author(s):  
Abdelraouf A Elmanama ◽  
Suhaila Al-Sheboul ◽  
Renad I Abu-Dan
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Antibiotic Resistance ◽  
Antimicrobial Resistance ◽  
Quorum Sensing ◽  
Bacterial Adhesion ◽  
Biofilm Formation ◽  
Bacterial Infections ◽  
Developmental Stages ◽  
Infection Site ◽  
Major Virulence Factor

Abstract Pseudomonas aeruginosa threatens patient’s care. It is considered as the most complicated health care associated pathogen to be eliminated from infection site. The biofilm forming ability of P. aeruginosa, being a major virulence factor for most pathogenic microorganism, protects it from host immunity and contribute to antibiotic resistance of this organism. It is estimated that about 80% of infectious diseases are due to biofilm mode of growth. Biofilm forming ability of bacteria imparts antimicrobial resistance that leads to many persistent and chronic bacterial infections. The world is becoming increasingly under the threat of entering the “post-antibiotic era”, an era in which the rate of death from bacterial infections is higher than from cancer. This review focus on P. aeruginosa biofilm forming ability; definition, developmental stages, and significance. In addition, the quorum sensing and the antibiotic resistance of this pathogen is discussed. Keywords: Biofilm; bacterial adhesion; Pseudomonas aeruginosa; antimicrobial resistance; quorum sensing.

scholarly journals Peptide Mix from Olivancillaria hiatula Interferes with Cell-to-Cell Communication in Pseudomonas aeruginosa

2019 ◽  
Vol 2019 ◽  
pp. 1-12
Author(s):  
Edward Ntim Gasu ◽  
Hubert Senanu Ahor ◽  
Lawrence Sheringham Borquaye
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Quorum Sensing ◽  
Biofilm Formation ◽  
Antimicrobial Agents ◽  
Cell Communication ◽  
Microtiter Plate ◽  
Antibiofilm Activity ◽  
Dependent Manner ◽  
Biofilm Inhibition ◽  
Swarming Motility

Bacteria in biofilms are encased in an extracellular polymeric matrix that limits exposure of microbial cells to lethal doses of antimicrobial agents, leading to resistance. In Pseudomonas aeruginosa, biofilm formation is regulated by cell-to-cell communication, called quorum sensing. Quorum sensing facilitates a variety of bacterial physiological functions such as swarming motility and protease, pyoverdine, and pyocyanin productions. Peptide mix from the marine mollusc, Olivancillaria hiatula, has been studied for its antibiofilm activity against Pseudomonas aeruginosa. Microscopy and microtiter plate-based assays were used to evaluate biofilm inhibitory activities. Effect of the peptide mix on quorum sensing-mediated processes was also evaluated. Peptide mix proved to be a good antibiofilm agent, requiring less than 39 μg/mL to inhibit 50% biofilm formation. Micrographs obtained confirmed biofilm inhibition at 1/2 MIC whereas 2.5 mg/mL was required to degrade preformed biofilm. There was a marked attenuation in quorum sensing-mediated phenotypes as well. At 1/2 MIC of peptide, the expression of pyocyanin, pyoverdine, and protease was inhibited by 60%, 72%, and 54%, respectively. Additionally, swarming motility was repressed by peptide in a dose-dependent manner. These results suggest that the peptide mix from Olivancillaria hiatula probably inhibits biofilm formation by interfering with cell-to-cell communication in Pseudomonas aeruginosa.

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