Inhibitory Effects of Cinnamaldehyde Derivatives on Biofilm Formation and Virulence Factors in Vibrio Species

Vibrio parahaemolyticus is considered one of the most relevant pathogenic marine bacteria with a range of virulence factors to establish food-related gastrointestinal infections in humans. Cinnamaldehyde (CNMA) and some of its derivatives have antimicrobial and antivirulence activities against several bacterial pathogens. This study examined the inhibitory effects of CNMA and its derivatives on biofilm formation and the virulence factors in Vibrio species, particularly V. parahaemolyticus. CNMA and ten of its derivatives were initially screened against V. parahaemolyticus biofilm formation, and their effects on the production of virulence factors and gene expression were studied. Among the CNMA derivatives tested, 4-nitrocinnamaldehyde, 4-chlorocinnamaldehyde, and 4-bromocinnamaldehyde displayed antibacterial and antivirulence activities, while the backbone CNMA had weak effects. The derivatives could prevent the adhesion of V. parahaemolyticus to surfaces by the dose-dependent inhibition of cell surface hydrophobicity, fimbriae production, and flagella-mediated swimming and swarming phenotypes. They also decreased the protease secretion required for virulence and indole production, which could act as an important signal molecule. The expression of QS and biofilm-related genes (aphA, cpsA, luxS, and opaR), virulence genes (fliA, tdh, and vopS), and membrane integrity genes (fadL, and nusA) were downregulated in V. parahaemolyticus by these three CNMA analogs. Interestingly, they eliminated V. parahaemolyticus and reduced the background flora from the squid surface. In addition, they exhibited similar antimicrobial and antibiofilm activities against Vibrio harveyi. This study identified CNMA derivatives as potential broad-spectrum antimicrobial agents to treat biofilm-mediated Vibrio infections and for surface disinfection in food processing facilities.

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Virulence Factors and Azole-Resistant Mechanism of Candida Tropicalis Isolated From Candidemia

10.21203/rs.3.rs-377398/v1 ◽

2021 ◽

Author(s):

Elahe Sasani ◽

Sadegh Khodavaisy ◽

Sassan Rezaie ◽

Mohammadreza Salehi ◽

Muhammad Getso ◽

...

Keyword(s):

Virulence Factors ◽

Candida Tropicalis ◽

Biofilm Formation ◽

Molecular Mechanisms ◽

Antifungal Susceptibility ◽

Cell Surface Hydrophobicity ◽

Surface Hydrophobicity ◽

Azole Resistance ◽

Virulence Determinants ◽

Fluconazole Resistant

Abstract Background Virulence factors intensify the pathogenicity of Candida species in candidemia. Limited knowledge exists regarding the azole-resistant mechanism and virulence factors of Candida tropicalis. Consequently, we aimed to evaluate the virulence factors and the molecular mechanisms of azole resistance among C. tropicalis isolated from bloodstream infection. Materials and methods Forty-five C. tropicalis isolates recovered from candidemia patients were evaluated for virulence factors, including extracellular enzymatic activities, cell surface hydrophobicity (CHS), and biofilm formation. Antifungal susceptibility pattern and expression level of ERG11, UPC2, MDR1, and CDR1 genes of eight azole resistance C. tropicalis isolates were assessed. Results The isolates expressed different frequencies of virulence determinants as follows: coagulase 4 (8.9%), phospholipase 4 (8.9 %), proteinase 31 (68.9 %), CSH 43 (95.6 %), esterase 43 (95.6 %), hemolysin 44 (97.8%), and biofilm formation 45 (100%). All the isolates were susceptible to amphotericin B and showed the highest resistance to voriconazole. The high expression of ERG11 and UPC2 genes in fluconazole-resistant C. tropicalis isolates were observed. Conclusion C. tropicalis isolated from candidemia patients extensively displayed capacities for biofilm formation, hemolysis, esterase activity, and hydrophobicity. In addition, the overexpression of ERG11 and UPC2 genes can be considered as one of the possible mechanisms of azole resistance.

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SubMICs of penicillin and erythromycin enhance biofilm formation and hydrophobicity of Corynebacterium diphtheriae strains

Journal of Medical Microbiology ◽

10.1099/jmm.0.052373-0 ◽

2013 ◽

Vol 62 (5) ◽

pp. 754-760 ◽

Cited By ~ 18

Author(s):

D. L. R. Gomes ◽

R. S. Peixoto ◽

E. A. B. Barbosa ◽

F. Napoleão ◽

P. S. Sabbadini ◽

...

Keyword(s):

Cell Surface ◽

Surface Properties ◽

Biofilm Formation ◽

Antimicrobial Agents ◽

Cell Surface Hydrophobicity ◽

Surface Hydrophobicity ◽

Corynebacterium Diphtheriae ◽

Surface Charges ◽

Bacterial Surface ◽

Bacterial Morphology

Subinhibitory concentrations (subMICs) of antibiotics may alter bacterial surface properties and change microbial physiology. This study aimed to investigate the effect of a subMIC (⅛ MIC) of penicillin (PEN) and erythromycin (ERY) on bacterial morphology, haemagglutinating activity, cell-surface hydrophobicity (CSH) and biofilm formation on glass and polystyrene surfaces, as well as the distribution of cell-surface acidic anionic residues of Corynebacterium diphtheriae strains (HC01 tox − strain; CDC-E8392 and 241 tox + strains). All micro-organisms tested were susceptible to PEN and ERY. Growth in the presence of PEN induced bacterial filamentation, whereas subMIC of ERY caused cell-size reduction of strains 241 and CDC-E8392. Adherence to human erythrocytes was reduced after growth in the presence of ERY, while CSH was increased by a subMIC of both antibiotics in bacterial adherence to n-hexadecane assays. Conversely, antibiotic inhibition of biofilm formation was not observed. All strains enhanced biofilm formation on glass after treatment with ERY, while only strain 241 increased glass adherence after cultivation in the presence of PEN. Biofilm production on polystyrene surfaces was improved by ⅛ MIC of ERY. After growth in the presence of both antimicrobial agents, strains 241 and CDC-E8392 exhibited anionic surface charges with focal distribution. In conclusion, subMICs of PEN and ERY modified bacterial surface properties and enhanced not only biofilm formation but also cell-surface hydrophobicity. Antibiotic-induced biofilm formation may contribute to the inconsistent success of antimicrobial therapy for C. diphtheriae infections.

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Evaluation of cell surface hydrophobicity and biofilm formation as pathogenic determinants among ESBL producing uropathogenic Escherichia coli

Indian Journal of Microbiology Research ◽

10.18231/j.ijmr.2021.054 ◽

2021 ◽

Vol 8 (4) ◽

pp. 263-267

Author(s):

Anandkumar H ◽

Amaresh Nigudgi ◽

Vinay Hajare ◽

Sunil Biradar

Keyword(s):

Cell Surface ◽

Biofilm Formation ◽

Antimicrobial Agents ◽

Critical Role ◽

Cell Surface Hydrophobicity ◽

Surface Hydrophobicity ◽

Adverse Outcomes ◽

Biofilm Production ◽

Significant Difference ◽

Esbl Producers

The attachment of the bacteria to the host cell and ability to invade the cell are regarded as important steps in the infectious process. The hydrophobicity of the microbial surface plays a critical role in the adherence of bacteria to the surface. The ability of biofilm formation can increase survival chance of microorganism, as cell growing in biofilm are highly resistant to the components of the immune system and many antimicrobial agents. Infection caused by ESBL- producers are associated with severe adverse outcomes and may be related to increased virulence of these strains.: A total of 100 urinary were selected for the study, of which 50 strains were from ESBL producers and 50 from non- ESBL-producing uropathogenic(UPEC) strains. The urinary isolates that were resistant to at least one of the three indicator cephalosporins (cefotaxime, cefpodoxime and ceftazidime) were tested for ESBL production by quantitative E-strip method. All the 100 urinary strains were tested for cell surface hydrophobicity (CSH) by salt aggregation method and Biofilm production by tissue culture plate method.Among ESBL producers, 19 (38%) were CSH positive and 34 (68%) were biofilm producers. However among non-ESBL producers, 05 (10%) were CSH positive and 12 (24%) were biofilm producers. Statistically significant difference (<0.001) was seen in the occurrence of CSH and biofilm production between ESBL and non ESBL producing UPEC isolates.In the present study, it was found that the ESBL producing isolates had a higher ability to form biofilm and CSH; both of them are among the important virulence factors associated with cell surface adherence which is the first step in bacterial infection.

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Cell surface hydrophobicity, biofilm formation, adhesives properties and molecular detection of adhesins genes in Staphylococcus aureus associated to dental caries

Microbial Pathogenesis ◽

10.1016/j.micpath.2010.03.007 ◽

2010 ◽

Vol 49 (1-2) ◽

pp. 14-22 ◽

Cited By ~ 58

Author(s):

Bochra Kouidhi ◽

Tarek Zmantar ◽

Hajer Hentati ◽

Amina Bakhrouf

Keyword(s):

Staphylococcus Aureus ◽

Dental Caries ◽

Cell Surface ◽

Biofilm Formation ◽

Molecular Detection ◽

Cell Surface Hydrophobicity ◽

Surface Hydrophobicity

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Quercetin inhibits virulence properties of Porphyromas gingivalis in periodontal disease

Scientific Reports ◽

10.1038/s41598-020-74977-y ◽

2020 ◽

Vol 10 (1) ◽

Author(s):

Zhiyan He ◽

Xu Zhang ◽

Zhongchen Song ◽

Lu Li ◽

Haishuang Chang ◽

...

Keyword(s):

Cell Surface ◽

Periodontal Disease ◽

Biofilm Formation ◽

Cell Structure ◽

Cell Surface Hydrophobicity ◽

Surface Hydrophobicity ◽

Laser Scanning Microscopy ◽

Confocal Laser ◽

Antimicrobial Effects ◽

Virulence Properties

Abstract Porphyromonas gingivalis is a causative agent in the onset and progression of periodontal disease. This study aims to investigate the effects of quercetin, a natural plant product, on P. gingivalis virulence properties including gingipain, haemagglutinin and biofilm formation. Antimicrobial effects and morphological changes of quercetin on P. gingivalis were detected. The effects of quercetin on gingipains activities and hemolytic, hemagglutination activities were evaluated using chromogenic peptides and sheep erythrocytes. The biofilm biomass and metabolism with different concentrations of quercetin were assessed by the crystal violet and MTT assay. The structures and thickness of the biofilms were observed by confocal laser scanning microscopy. Bacterial cell surface properties including cell surface hydrophobicity and aggregation were also evaluated. The mRNA expression of virulence and iron/heme utilization was assessed using real time-PCR. Quercetin exhibited antimicrobial effects and damaged the cell structure. Quercetin can inhibit gingipains, hemolytic, hemagglutination activities and biofilm formation at sub-MIC concentrations. Molecular docking analysis further indicated that quercetin can interact with gingipains. The biofilm became sparser and thinner after quercetin treatment. Quercetin also modulate cell surface hydrophobicity and aggregation. Expression of the genes tested was down-regulated in the presence of quercetin. In conclusion, our study demonstrated that quercetin inhibited various virulence factors of P. gingivalis.

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Recombinant N-acyl homoserine lactone-Lactonase AiiAQSI-1 Attenuates Aeromonas hydrophila Virulence Factors, Biofilm Formation and Reduces Mortality in Crucian Carp

Marine Drugs ◽

10.3390/md17090499 ◽

2019 ◽

Vol 17 (9) ◽

pp. 499 ◽

Cited By ~ 2

Author(s):

Bao Zhang ◽

Xiyi Zhuang ◽

Liyun Guo ◽

Robert J. C. McLean ◽

Weihua Chu

Keyword(s):

Virulence Factors ◽

Aeromonas Hydrophila ◽

Biofilm Formation ◽

Crucian Carp ◽

Homoserine Lactone ◽

In Vivo Studies ◽

Acyl Homoserine Lactone ◽

Signal Molecule ◽

Promising Alternative ◽

Feed Supplementation

Quorum quenching (QQ) is a promising alternative infection-control strategy to antibiotics that controls quorum-regulated virulence without killing the pathogens. Aeromonas hydrophila is an opportunistic gram-negative pathogen living in freshwater and marine environments. A. hydrophila possesses an N-acyl homoserine lactone (AHL)-based quorum-sensing (QS) system that regulates virulence, so quorum signal-inactivation (i.e., QQ) may represent a new way to combat A. hydrophila infection. In this study, an AHL lactonase gene, aiiA was cloned from Bacillus sp. strain QSI-1 and expressed in Escherichia coli strain BL21(DE3). The A. hydrophila hexanoyl homoserine lactone (C6-HSL) QS signal molecule was degraded by AiiAQSI-1, which resulted in a decrease of bacterial swimming motility, reduction of extracellular protease and hemolysin virulence factors, and inhibited the biofilm formation of A. hydrophila YJ-1 in a microtiter assay. In cell culture studies, AiiAQSI-1 decreased the ability of A. hydrophila adherence to and internalization by Epithelioma papulosum cyprini (EPC) cells. During in vivo studies, oral administration of AiiAQSI-1 via feed supplementation attenuated A. hydrophila infection in Crucian Carp. Results from this work indicate that feed supplementation with AiiAQSI-1 protein has potential to control A. hydrophila aquaculture disease via QQ.

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Baicalein Inhibits Streptococcus mutans Biofilms and Dental Caries-Related Virulence Phenotypes

Antibiotics ◽

10.3390/antibiotics10020215 ◽

2021 ◽

Vol 10 (2) ◽

pp. 215

Author(s):

Aparna Vijayakumar ◽

Hema Bhagavathi Sarveswari ◽

Sahana Vasudevan ◽

Karthi Shanmugam ◽

Adline Princy Solomon ◽

...

Keyword(s):

Dental Caries ◽

Streptococcus Mutans ◽

Biofilm Formation ◽

Acid Production ◽

Cell Surface Hydrophobicity ◽

Surface Hydrophobicity ◽

Oral Disease ◽

Public Healthcare ◽

Surface Attachment ◽

First Time

Dental caries, the most common oral disease, is a major public healthcare burden and affects more than three billion people worldwide. The contemporary understanding of the need for a healthy microbiome and the emergence of antimicrobial resistance has resulted in an urgent need to identify compounds that curb the virulence of pathobionts without microbial killing. Through this study, we have demonstrated for the first time that 5,6,7-trihydroxyflavone (Baicalein) significantly downregulates crucial caries-related virulence phenotypes in Streptococcus mutans. Baicalein significantly inhibited biofilm formation by Streptococcus mutans UA159 (MBIC50 = 200 μM), without significant growth inhibition. Notably, these concentrations of baicalein did not affect the commensal S. gordonii. Strikingly, baicalein significantly reduced cell surface hydrophobicity, autoaggregation and acid production by S. mutans. Mechanistic studies (qRT-PCR) showed downregulation of various genes regulating biofilm formation, surface attachment, quorum sensing, acid production and competence. Finally, we demonstrate the potential translational value of baicalein by reporting synergistic interaction with fluoride against S. mutans biofilms.

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Effect of Eugenol on Cell Surface Hydrophobicity, Adhesion, and Biofilm ofCandida tropicalisandCandida dubliniensisIsolated from Oral Cavity of HIV-Infected Patients

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2014/505204 ◽

2014 ◽

Vol 2014 ◽

pp. 1-8 ◽

Cited By ~ 20

Author(s):

Suelen Balero de Paula ◽

Thais Fernanda Bartelli ◽

Vanessa Di Raimo ◽

Jussevania Pereira Santos ◽

Alexandre Tadachi Morey ◽

...

Keyword(s):

Cell Surface ◽

Oral Cavity ◽

Biofilm Formation ◽

Cell Surface Hydrophobicity ◽

Surface Hydrophobicity ◽

Planktonic Cells ◽

Hydrophobic Behavior ◽

Significant Difference ◽

Substrate Surfaces ◽

Sessile Cells

MostCandidaspp. infections are associated with biofilm formation on host surfaces. Cells within these communities display a phenotype resistant to antimicrobials and host defenses, so biofilm-associated infections are difficult to treat, representing a source of reinfections. The present study evaluated the effect of eugenol on the adherence properties and biofilm formation capacity ofCandida dubliniensisandCandida tropicalisisolated from the oral cavity of HIV-infected patients. All isolates were able to form biofilms on different substrate surfaces. Eugenol showed inhibitory activity against planktonic and sessile cells ofCandidaspp. No metabolic activity in biofilm was detected after 24 h of treatment. Scanning electron microscopy demonstrated that eugenol drastically reduced the number of sessile cells on denture material surfaces. MostCandidaspecies showed hydrophobic behavior and a significant difference in cell surface hydrophobicity was observed after exposure of planktonic cells to eugenol for 1 h. Eugenol also caused a significant reduction in adhesion of mostCandidaspp. to HEp-2 cells and to polystyrene. These findings corroborate the effectiveness of eugenol againstCandidaspecies other thanC. albicans, reinforcing its potential as an antifungal applied to limit both the growth of planktonic cells and biofilm formation on different surfaces.

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