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 Efficacy of Synthetic Furanones on Listeria monocytogenes Biofilm Formation

Foods ◽  
2019 ◽  
Vol 8 (12) ◽  
pp. 647 ◽  
Author(s):  
Pedro Rodríguez-López ◽  
Andrea Emparanza Barrenengoa ◽  
Sergio Pascual-Sáez ◽  
Marta López Cabo
Keyword(s):  
Listeria Monocytogenes ◽  
Biofilm Formation ◽  
Epifluorescence Microscopy ◽  
Dependent Manner ◽  
Antifouling Activity ◽  
Aisi 316 ◽  
Novel Strategy ◽  
And Control ◽  
Acylated Homoserine Lactones ◽  
Dose Dependent

Furanones are analogues of acylated homoserine lactones with proven antifouling activity in both Gram-positive and Gram-negative bacteria though the interference of various quorum sensing pathways. In an attempt to find new strategies to prevent and control Listeria monocytogenes biofilm formation on stainless steel (SS) surfaces, different concentrations of six synthetic furanones were applied on biofilms formed by strains isolated from food, environmental, and clinical sources grown onto AISI 316 SS coupons. Among the furanones tested, (Z-)-4-Bromo-5-(bromomethylene)-2(5H)-furanone and 3,4-Dichloro-2(5H)-furanone significantly (p < 0.05) reduced the adhesion capacity (>1 log CFU cm−2) in 24 h treated biofilms. Moreover, individually conducted experiments demonstrated that (Z-)-4-Bromo-5-(bromomethylene)-2(5H)-furanone was able to not only significantly (p < 0.05) prevent L. monocytogenes adhesion but also to reduce the growth rate of planktonic cells up to 48 h in a dose-dependent manner. LIVE/DEAD staining followed by epifluorescence microscopy visualisation confirmed these results show an alteration of the structure of the biofilm in furanone-treated samples. Additionally, it was demonstrated that 20 µmol L−1 of 3,4-Dichloro-2(5H)-furanone dosed at 0, 24 and 96 h was able to maintain a lower level of adhered cells (>1 log CFU cm−2; p < 0.05). Since furanones do not pose a selective pressure on bacteria, these results represent an appealing novel strategy for the prevention of L. monocytogenes biofilm grown onto SS.

scholarly journals Enhancement of Biofilm Formation by Subinhibitory Concentrations of Macrolides in icaADBC-Positive and -Negative Clinical Isolates of Staphylococcus epidermidis

2010 ◽  
Vol 54 (6) ◽  
pp. 2707-2711 ◽  
Author(s):  
Qian Wang ◽  
Feng-Jun Sun ◽  
Yao Liu ◽  
Li-Rong Xiong ◽  
Lin-Li Xie ◽  
...  
Keyword(s):  
Staphylococcus Epidermidis ◽  
Clinical Relevance ◽  
Biofilm Formation ◽  
Clinical Isolates ◽  
Dependent Manner ◽  
Biofilm Growth ◽  
Subinhibitory Concentrations ◽  
Dose Dependent

ABSTRACT Biofilm formation in Staphylococcus epidermidis is mediated by icaADBC-dependent and -independent pathways. Subinhibitory concentrations of erythromycin, azithromycin, and clarithromycin enhanced, in a dose-dependent manner, the level of biofilm formation by 20% (21/105 isolates) by macrolide-resistant ica-positive and -negative isolates tested in vitro. The presence of ica, however, apparently produced an enhanced effect on biofilm formation. The levels of expression of the biofilm-related genes icaA, atlE, fruA, pyrR, sarA, and sigB were increased in response to erythromycin. The results likely underscore the potential clinical relevance of macrolide-induced biofilm growth.

Growth inhibition of adherent Pseudomonas aeruginosa by an N-butanoyl-l-homoserine lactone analog

2010 ◽  
Vol 56 (4) ◽  
pp. 317-325 ◽  
Author(s):  
Pouneh Khalilzadeh ◽  
Barbora Lajoie ◽  
Salomé El Hage ◽  
Aurélie Furiga ◽  
Geneviève Baziard ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Biofilm Formation ◽  
Communication Systems ◽  
Homoserine Lactone ◽  
Adherent Cells ◽  
Dependent Manner ◽  
Structure Activity ◽  
Opportunistic Human Pathogen ◽  
Dose Dependent ◽  
Related Compounds

The discovery of quorum sensing (QS) communication systems regulating bacterial virulence has afforded a novel opportunity for controlling infectious bacteria by interfering with QS. Pseudomonas aeruginosa is an example of an opportunistic human pathogen for which N-acyl homoserine lactone (AHL)-related compounds have been described as potent inhibitors of biofilm formation and virulence factors, given their similarity to the natural QS autoinducers (AHLs). Our purpose was to design potent analogs of N-butanoyl-l-homoserine lactone (C4-HSL) and to screen them for biological activity. Eleven original compounds characterized by the modification of the lactone moiety were screened for their ability to impair biofilm formation. Among them, compound 11 was able to modify the growth kinetics and to restrict the number of adherent cells when added from the early stages of biofilm formation (i.e., adhesion and microcolony formation) in a dose-dependent manner. To demonstrate antagonism with C4-HSL, we showed that the inhibition of biofilm formation by compound 11 was impaired when C4-HSL was added. Structure–activity relationships are discussed with respect to the results obtained.

Inhibitors of bacterial H2S biogenesis targeting antibiotic resistance and tolerance

Science ◽  
2021 ◽  
Vol 372 (6547) ◽  
pp. 1169-1175
Author(s):  
Konstantin Shatalin ◽  
Ashok Nuthanakanti ◽  
Abhishek Kaushik ◽  
Dmitry Shishov ◽  
Alla Peselis ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Pseudomonas Aeruginosa ◽  
Antibiotic Resistance ◽  
Hydrogen Sulfide ◽  
Small Molecules ◽  
Biofilm Formation ◽  
Drug Target ◽  
Human Pathogens ◽  
Defense System

Emergent resistance to all clinical antibiotics calls for the next generation of therapeutics. Here we report an effective antimicrobial strategy targeting the bacterial hydrogen sulfide (H2S)–mediated defense system. We identified cystathionine γ-lyase (CSE) as the primary generator of H2S in two major human pathogens, Staphylococcus aureus and Pseudomonas aeruginosa, and discovered small molecules that inhibit bacterial CSE. These inhibitors potentiate bactericidal antibiotics against both pathogens in vitro and in mouse models of infection. CSE inhibitors also suppress bacterial tolerance, disrupting biofilm formation and substantially reducing the number of persister bacteria that survive antibiotic treatment. Our results establish bacterial H2S as a multifunctional defense factor and CSE as a drug target for versatile antibiotic enhancers.

scholarly journals No Correlation between Biofilm Formation, Virulence Factors, and Antibiotic Resistance in Pseudomonas aeruginosa: Results from a Laboratory-Based In Vitro Study

Antibiotics ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 1134
Author(s):  
Márió Gajdács ◽  
Zoltán Baráth ◽  
Krisztina Kárpáti ◽  
Dóra Szabó ◽  
Donatella Usai ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Antibiotic Resistance ◽  
Virulence Factors ◽  
Biofilm Formation ◽  
Bacterial Infections ◽  
Pearson Correlation ◽  
Pigment Production ◽  
Virulence Determinants ◽  
Secretion Systems

Pseudomonas aeruginosa (P. aeruginosa) possesses a plethora of virulence determinants, including the production of biofilm, pigments, exotoxins, proteases, flagella, and secretion systems. The aim of our present study was to establish the relationship between biofilm-forming capacity, the expression of some important virulence factors, and the multidrug-resistant (MDR) phenotype in P. aeruginosa. A total of three hundred and two (n = 302) isolates were included in this study. Antimicrobial susceptibility testing and phenotypic detection of resistance determinants were carried out; based on these results, isolates were grouped into distinct resistotypes and multiple antibiotic resistance (MAR) indices were calculated. The capacity of isolates to produce biofilm was assessed using a crystal violet microtiter-plate based method. Motility (swimming, swarming, and twitching) and pigment-production (pyoverdine and pyocyanin) were also measured. Pearson correlation coefficients (r) were calculated to determine for antimicrobial resistance, biofilm-formation, and expression of other virulence factors. Resistance rates were the highest for ceftazidime (56.95%; n = 172), levofloxacin (54.97%; n = 166), and ciprofloxacin (54.64%; n = 159), while lowest for colistin (1.66%; n = 5); 44.04% (n = 133) of isolates were classified as MDR. 19.87% (n = 60), 20.86% (n = 63) and 59.27% (n = 179) were classified as weak, moderate, and strong biofilm producers, respectively. With the exception of pyocyanin production (0.371 ± 0.193 vs. non-MDR: 0.319 ± 0.191; p = 0.018), MDR and non-MDR isolates did not show significant differences in expression of virulence factors. Additionally, no relevant correlations were seen between the rate of biofilm formation, pigment production, or motility. Data on interplay between the presence and mechanisms of drug resistance with those of biofilm formation and virulence is crucial to address chronic bacterial infections and to provide strategies for their management.

scholarly journals Ginsenoside-Rb1 Protects Hypoxic- and Ischemic-Damaged Cardiomyocytes by Regulating Expression of miRNAs

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Xu Yan ◽  
Jinrong Xue ◽  
Hongjin Wu ◽  
Shengqi Wang ◽  
Yuna Liu ◽  
...  
Keyword(s):  
Neonatal Rat ◽  
Control Group ◽  
Dependent Manner ◽  
The Novel ◽  
Rat Cardiomyocytes ◽  
Neonatal Rat Cardiomyocytes ◽  
Proliferation And Apoptosis ◽  
Novel Strategy ◽  
Dose Dependent

Ginsenoside (GS-Rb1) is one of the most important active compounds of ginseng, with extensive evidence of its cardioprotective properties. However, the miRNA mediated mechanism of GS-Rb1 on cardiomyocytes remains unclear. Here, the roles of miRNAs in cardioprotective activity of GS-Rb1 were investigated in hypoxic- and ischemic-damaged cardiomyocytes. Neonatal rat cardiomyocytes (NRCMs) were first isolated, cultured, and then incubated with or without GS-Rb1 (2.5–40μM)in vitrounder conditions of hypoxia and ischemia. Cell growth, proliferation, and apoptosis were detected by MTT and flow cytometry. Expressions of various microRNAs were analyzed by real-time PCR. Compared with that of the control group, GS-Rb1 significantly decreased cell death in a dose-dependent manner and expressions of mir-1, mir-29a, and mir-208 obviously increased in the experimental model groups. In contrast, expressions of mir-21 and mir-320 were significantly downregulated and GS-Rb1 could reverse the differences in a certain extent. The miRNAs might be involved in the protective effect of GS-Rb1 on the hypoxia/ischemia injuries in cardiomyocytes. The effect might be based on the upregulation of mir-1, mir-29a, and mir-208 and downregulation of mir-21 and mir-320. This might provide us a new target to explore the novel strategy for ischemic cardioprotection.

scholarly journals Polymer-directed inhibition of reversible to irreversible attachment prevents Pseudomonas aeruginosa biofilm formation

2022 ◽  
Author(s):  
Alessandro Carabelli ◽  
Jean-Frederic Dubern ◽  
Maria Papangeli ◽  
Nicola E. Farthing ◽  
Olutoba Sanni ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Biofilm Formation ◽  
Cell Tracking ◽  
Constitutive Expression ◽  
Bacterial Biofilm ◽  
Dependent Manner ◽  
Type Iv ◽  
Controlled Flow

Non-toxic, biocompatible materials that inhibit bacterial biofilm formation on implanted medical devices and so prevent infection are urgently required. Weakly amphiphilic acrylate polymers with rigid hydrocarbon pendant groups resist bacterial biofilm formation in vitro and in vivo but the biological mechanism involved is not known. By comparing biofilm formation on polymers with the same acrylate backbone but with different pendant groups, we show that poly(ethylene glycol dicyclopentenyl ether acrylate; pEGdPEA) but not neopentyl glycol propoxylate diacrylate (pNGPDA) inhibited the transition from reversible to irreversible attachment. By using single-cell tracking algorithms and controlled flow microscopy we observed that fewer Pseudomonas aeruginosa PAO1 cells accumulated on pEGdPEA compared with pNGPDA. Bacteria reaching the pEGdPEA surface exhibited shorter residence times and greater asymmetric division with more cells departing from the surface post-cell division, characteristic of reversible attachment. Migrating cells on pEGdPEA deposited fewer exopolysaccharide trails and were unable top adhere strongly. Discrimination between the polymers required type IV pili and flagella. On pEGdPEA, the lack of accumulation of cyclic diguanylate or expression of sadB were consistent with the failure to transit from reversible to irreversible attachment. Constitutive expression of sadB increased surface adhesion sufficient to enable P. aeruginosa to form biofilms in a Mot flagellar stator dependent manner. These findings were extendable to other biofilm resistant acrylates highlighting their unique ability to inhibit reversible to irreversible attachment as a mechanism for preventing biofilm-associated infections.

scholarly journals Fibrinogen Induces Biofilm Formation by Streptococcus suis and Enhances Its Antibiotic Resistance

2008 ◽  
Vol 74 (15) ◽  
pp. 4969-4972 ◽  
Author(s):  
Laetitia Bonifait ◽  
Louis Grignon ◽  
Daniel Grenier
Keyword(s):  
Antibiotic Resistance ◽  
Biofilm Formation ◽  
Culture Medium ◽  
Streptococcus Suis ◽  
Penicillin G ◽  
Dependent Manner ◽  
Planktonic Cells ◽  
Dose Dependent

ABSTRACT In this study, we showed that supplementing the culture medium with fibrinogen induced biofilm formation by Streptococcus suis in a dose-dependent manner. Biofilm-grown S. suis cells were much more resistant to penicillin G than planktonic cells. S. suis bound fibrinogen to its surface, a property that likely contributes to biofilm formation.

Oxygenation of 18-hydroxycorticosterone as the final reaction for aldosterone biosynthesis

1984 ◽  
Vol 107 (3) ◽  
pp. 395-400 ◽  
Author(s):  
Itaru Kojima ◽  
Etsuro Ogata ◽  
Hiroshi Inano ◽  
Bun-ichi Tamaoki
Keyword(s):  
Carbon Monoxide ◽  
Hydroxysteroid Dehydrogenase ◽  
Dependent Manner ◽  
In Vitro Production ◽  
Mitochondrial Preparation ◽  
Final Reaction ◽  
Vitro Production ◽  
Dose Dependent ◽  
Cytochrome P 450

Abstract. Incubation of 18-hydroxycorticosterone with the sonicated mitochondrial preparation of bovine adrenal glomerulosa tissue leads to the production of aldosterone, as measured by radioimmunoassay. The in vitro production of aldosterone from 18-hydroxycorticosterone requires both molecular oxygen and NADPH, and is inhibited by carbon monoxide. Cytochrome P-450 inhibitors such as metyrapone, SU 8000. SU 10603, SKF 525A, amphenone B and spironolactone decrease the biosynthesis of aldosterone from 18-hydroxycorticosterone. These results support the conclusion that the final reaction in aldosterone synthesis from 18-hydroxycorticosterone is catalyzed by an oxygenase, but not by 18-hydroxysteroid dehydrogenase. By the same preparation, the production of [3H]aldosterone but not [3H]18-hydroxycorticosterone from [1,2-3H ]corticosterone is decreased in a dose-dependent manner by addition of non-radioactive 18-hydroxycorticosterone.

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