scholarly journals Multivalency effects on Pseudomonas aeruginosa biofilm inhibition and dispersal by glycopeptide dendrimers targeting lectin LecA

2016 ◽  
Vol 14 (1) ◽  
pp. 138-148 ◽  
Author(s):  
Myriam Bergmann ◽  
Gaëlle Michaud ◽  
Ricardo Visini ◽  
Xian Jin ◽  
Emilie Gillon ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Biofilm Inhibition ◽  
Convergent Synthesis ◽  
Peptide Dendrimer ◽  
Dispersal Activity

The octagalactosylated G3 peptide dendrimer GalAxG3 was obtained by convergent synthesis, bound tightly to lectin LecA, and showed strong Pseudomonas aerguinosa biofilm inhibition and dispersal activity.

scholarly journals Effect of Nitroxides on Swarming Motility and Biofilm Formation, Multicellular Behaviors in Pseudomonas aeruginosa

2013 ◽  
Vol 57 (10) ◽  
pp. 4877-4881 ◽  
Author(s):  
César de la Fuente-Núñez ◽  
Fany Reffuveille ◽  
Kathryn E. Fairfull-Smith ◽  
Robert E. W. Hancock
Keyword(s):  
Nitric Oxide ◽  
Pseudomonas Aeruginosa ◽  
Biofilm Formation ◽  
Wild Type ◽  
Planktonic Cells ◽  
Swarming Motility ◽  
Content Type ◽  
Exogenous Addition ◽  
Biofilm Dispersion ◽  
Dispersal Activity

ABSTRACTThe ability of nitric oxide (NO) to induce biofilm dispersion has been well established. Here, we investigated the effect of nitroxides (sterically hindered nitric oxide analogues) on biofilm formation and swarming motility inPseudomonas aeruginosa. A transposon mutant unable to produce nitric oxide endogenously (nirS) was deficient in swarming motility relative to the wild type and the complemented strain. Moreover, expression of thenirSgene was upregulated by 9.65-fold in wild-type swarming cells compared to planktonic cells. Wild-type swarming levels were substantially restored upon the exogenous addition of nitroxide containing compounds, a finding consistent with the hypothesis that NO is necessary for swarming motility. Here, we showed that nitroxides not only mimicked the dispersal activity of NO but also prevented biofilms from forming in flow cell chambers. In addition, anirStransposon mutant was deficient in biofilm formation relative to the wild type and the complemented strain, thus implicating NO in the formation of biofilms. Intriguingly, despite its stand-alone action in inhibiting biofilm formation and promoting dispersal, a nitroxide partially restored the ability of anirSmutant to form biofilms.

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.

Pseudomonas aeruginosa Quorum Sensing and Biofilm Inhibition

2019 ◽  
pp. 227-256 ◽  
Author(s):  
Barış Gökalsın ◽  
Didem Berber ◽  
Nüzhet Cenk Sesal
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Quorum Sensing ◽  
Biofilm Inhibition

Iron-binding compounds impair Pseudomonas aeruginosa biofilm formation, especially under anaerobic conditions

2009 ◽  
Vol 58 (6) ◽  
pp. 765-773 ◽  
Author(s):  
Che Y. O'May ◽  
Kevin Sanderson ◽  
Louise F. Roddam ◽  
Sylvia M. Kirov ◽  
David W. Reid
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Biofilm Formation ◽  
Low Oxygen ◽  
Anaerobic Conditions ◽  
Chronic Infections ◽  
Strain Pao1 ◽  
Biofilm Inhibition ◽  
Oxygen Conditions ◽  
Biofilm Development ◽  
Chelating Compounds

The success of Pseudomonas aeruginosa in cystic fibrosis (CF) and other chronic infections is largely attributed to its ability to grow in antibiotic-resistant biofilm communities. This study investigated the effects of limiting iron levels as a strategy for preventing/disrupting P. aeruginosa biofilms. A range of synthetic and naturally occurring iron-chelating agents were examined. Biofilm development by P. aeruginosa strain PAO1 and CF sputum isolates from chronically infected individuals was significantly decreased by iron removal under aerobic atmospheres. CF strains formed poor biofilms under anaerobic conditions. Strain PAO1 was also tested under anaerobic conditions. Biofilm formation by this model strain was almost totally prevented by several of the chelators tested. The ability of synthetic chelators to impair biofilm formation could be reversed by iron addition to cultures, providing evidence that these effective chelating compounds functioned by directly reducing availability of iron to P. aeruginosa. In contrast, the biological chelator lactoferrin demonstrated enhanced anti-biofilm effects as iron supplementation increased. Hence biofilm inhibition by lactoferrin appeared to occur through more complex mechanisms to those of the synthetic chelators. Overall, our results demonstrate the importance of iron availability to biofilms and that iron chelators have potential as adjunct therapies for preventing biofilm development, especially under low oxygen conditions such as encountered in the chronically infected CF lung.

scholarly journals Pseudomonas aeruginosa Exopolysaccharide Psl Promotes Resistance to the Biofilm Inhibitor Polysorbate 80

2012 ◽  
Vol 56 (8) ◽  
pp. 4112-4122 ◽  
Author(s):  
Michael E. Zegans ◽  
Daniel Wozniak ◽  
Edward Griffin ◽  
Christine M. Toutain-Kidd ◽  
John H. Hammond ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Nonionic Surfactant ◽  
Biofilm Formation ◽  
Laboratory Strain ◽  
Polysorbate 80 ◽  
Biosynthetic Pathways ◽  
Human Tissues ◽  
Biofilm Inhibition ◽  
Content Type ◽  
Biofilm Inhibitor

ABSTRACTPolysorbate 80 (PS80) is a nonionic surfactant and detergent that inhibits biofilm formation byPseudomonas aeruginosaat concentrations as low as 0.001% and is well tolerated in human tissues. However, certain clinical and laboratory strains (PAO1) ofP. aeruginosaare able to form biofilms in the presence of PS80. To better understand this resistance, we performed transposon mutagenesis with a PS80-resistant clinical isolate, PA738. This revealed that mutation ofalgCrendered PA738 sensitive to PS80 biofilm inhibition. AlgC contributes to the biosynthesis of the exopolysaccharides Psl and alginate, as well as lipopolysaccharide and rhamnolipid. Analysis of mutations downstream of AlgC in these biosynthetic pathways established that disruption of thepsloperon was sufficient to render the PA738 and PAO1 strains sensitive to PS80-mediated biofilm inhibition. Increased levels of Psl production in the presence of arabinose in a strain with an arabinose-induciblepslpromoter were correlated with increased biofilm formation in PS80. InP. aeruginosastrains MJK8 and ZK2870, known to produce both Pel and Psl, disruption of genes in thepslbut not thepeloperon conferred susceptibility to PS80-mediated biofilm inhibition. The laboratory strain PA14 does not produce Psl and does not form biofilms in PS80. However, when PA14 was transformed with a cosmid containing thepsloperon, it formed biofilms in the presence of PS80. Taken together, these data suggest that production of the exopolysaccharide Psl byP. aeruginosapromotes resistance to the biofilm inhibitor PS80.

scholarly journals Identification of Peptides Derived from the Human Antimicrobial Peptide LL-37 Active against Biofilms Formed by Pseudomonas aeruginosa Using a Library of Truncated Fragments

2012 ◽  
Vol 56 (11) ◽  
pp. 5698-5708 ◽  
Author(s):  
C. Nagant ◽  
B. Pitts ◽  
K. Nazmi ◽  
M. Vandenbranden ◽  
J. G. Bolscher ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Antimicrobial Peptide ◽  
Eukaryotic Cells ◽  
Mitochondrial Activity ◽  
Antibiofilm Activity ◽  
Peptide Fragments ◽  
Biofilm Inhibition ◽  
Content Type ◽  
Amino Acid Peptide ◽  
Α Helix

ABSTRACTPersistentPseudomonas aeruginosainfections are a major cause of morbidity and mortality in cystic fibrosis (CF) patients and are linked to the formation of a biofilm. The development of new biofilm inhibition strategies is thus a major challenge. LL-37 is the only human antimicrobial peptide derived from cathelicidin. The effects on theP. aeruginosaPAO1 strain of synthetic truncated fragments of this peptide were compared with the effects of the original peptide. Fragments of LL-37 composed of 19 residues (LL-19, LL13-31, and LL7-25) inhibited biofilm formation. The strongest antibiofilm activity was observed with the peptides LL7-37 and LL-31, which decreased the percentage of biomass formation at a very low concentration. Some peptides were also active on the bacteria within an established biofilm. LL7-31, LL-31, and LL7-37 increased the uptake of propidium iodide (PI) by sessile bacteria. The peptide LL7-37 decreased the height of the biofilm and partly disrupted it. The peptides active within the biofilm had an infrared spectrum compatible with an α-helix. LL-37, but not the peptides LL7-31 and LL7-37, showed cellular toxicity by permeabilizing the eukaryotic plasma membrane (uptake of ethidium bromide and release of lactate dehydrogenase [LDH]). None of the tested peptides affected mitochondrial activity in eukaryotic cells. In conclusion, a 25-amino-acid peptide (LL7-31) displayed both strong antimicrobial and antibiofilm activities. The peptide was even active on cells within a preformed biofilm and had reduced toxicity toward eukaryotic cells. Our results also suggest the contribution of secondary structures (α-helix) to the activity of the peptides on biofilms.

scholarly journals Biofilm inhibitor taurolithocholic acid alters colony morphology, specialized metabolism, and virulence ofPseudomonas aeruginosa

2019 ◽  
Author(s):  
Alanna R. Condren ◽  
Lisa Juliane Kahl ◽  
George Kritikos ◽  
Manuel Banzhaf ◽  
Lars E. P. Dietrich ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Bacterial Community ◽  
Biofilm Formation ◽  
Colony Morphology ◽  
Biofilm Inhibition ◽  
Specialized Metabolism ◽  
Virulence Assay ◽  
Biofilm Inhibitor ◽  
Highly Virulent ◽  
Wax Moth

AbstractBiofilm inhibition by exogenous molecules has been an attractive strategy for the development of novel therapeutics. We investigated the biofilm inhibitor taurolithocholic acid (TLCA) and its effects on the specialized metabolism, virulence and biofilm formation of the clinically relevant bacteriumPseudomonas aeruginosastrain PA14. Our study shows that TLCA alters specialized metabolism, thereby affectingP. aeruginosacolony biofilm physiology. We observed an upregulation of metabolites correlated to virulence such as the siderophore pyochelin. A wax moth virulence assay confirmed that treatment with TLCA increases virulence ofP. aeruginosa. Based on our results, we believe that future endeavors to identify biofilm inhibitors must consider how a putative lead is altering the specialized metabolism of a bacterial community to prevent pathogens from entering a highly virulent state.

scholarly journals Synergistic effects of antimicrobial peptide dendrimer-chitosan polymer conjugates against Pseudomonas aeruginosa

2021 ◽  
pp. 119025
Author(s):  
Viorica Patrulea ◽  
Bee-Ha Gan ◽  
Karl Perron ◽  
Xingguang Cai ◽  
Philippe Abdel-Sayed ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Antimicrobial Peptide ◽  
Synergistic Effects ◽  
Polymer Conjugates ◽  
Peptide Dendrimer

Antibacterial and antibiofilm activity of the bacteriocin-producing strain Leuconostoc mesenteroides CHBY46 isolated from Algerian dromedary milk against Pseudomonas aeruginosa and Staphylococcus aureus biofilms

2019 ◽  
Vol 8 (4) ◽  
pp. 120-131
Author(s):  
Yahia Bellil ◽  
Zineb Benmechernene ◽  
Wassila Chahrour Bellil ◽  
Mebrouk Kihal
Keyword(s):  
Staphylococcus Aureus ◽  
Pseudomonas Aeruginosa ◽  
16S Rrna Gene Sequencing ◽  
Antibiofilm Activity ◽  
Rrna Gene ◽  
Biofilm Inhibition ◽  
Staph Aureus ◽  
Spoilage Bacteria ◽  
Dromedary Milk ◽  
And Staphylococcus Aureus

In order to control biofilm formation of pathogenic and spoilage bacteria in foods, some species of Leuconostoc are very important in food industries, as they increase the shelf life of foods during preservation. In this study the strain CHBY46 a bacteriocin-producing strain belonging to Leuconostoc ge-nus isolated from dromedary milk in the south of Algeria was characterized by 16S rRNA gene sequencing and MALDITOF MS mass spectrometry, tested for its antibacterial and antibiofilm activities against Pseudomonas aeruginosa and Staphylococcus aureus. The produced bacteriocin was partially puri-fied with sulfate ammonium precipitation and RP-HPLC. The strain CHBY46 was classified as Leuc. mesenteroides after molecular identification. Among the bacteria tested the pathogens Staph. aureus ATCC 29213 and Ps. aeru-ginosa ATCC 27653 were sensitive to this bacteriocin with 480 AU/ml. Antibi-ofilm activity was investigated by crystal violet assay. The bacteriocin of Leuc. mesenteroides CHBY 46 exhibited significant biofilm inhibition ; 35.58% with Ps. aeruginosa, and 42.11% with Staph. aureus. Tricine-SDS-PAGE analysis of the partially purified bacteriocin indicated a low molecular weight of approximately 3.5 kDa. Therfore, we conclude that bacteriocins from Leuco-nostoc have the potential as a therapeutic strategy against pathogen’s bio-films, which contribute, to bacterial pathogenicity and resistance toward antibiotics or being used in foods as adjunsts to contribute food safety.

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