Evaluation of the role of SsaV Salmonella pathogenicity island-2 dependent type III secretion system components on the virulence behavior of Salmonella enterica serovar Typhimurium

Hegazy, Wael A. H.; Abbas, Hisham A.

doi:10.5897/ajb2016.15852

Cited by 34 publications

(16 citation statements)

References 26 publications

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“…In sequential manner and after bacterial adhesion to surfaces, free floating vegetative cells start to produce extracellular polymeric substances which leads to irreversible attachment and entrapping of bacteria in biofilms [52]. The flagella-driven motilities are needed for P. mirabilis adhesion, which followed by its colonization and biofilm formation [49,53,54]. In compliance with our previous findings that showed the inhibition effect of metronidazole on P. mirabilis motilities; metronidazole is significantly reduced the adhesion of P. mirabilis to both abiotic surfaces and epithelial cells and also significantly decreased the biofilm formation.…”

Section: Mics and Mbecs Of Tested Antibiotics In Precence Of Metronidazole In Sub-micmentioning

confidence: 99%

Not Only Antimicrobial: Metronidazole Mitigates the Virulence of Proteus mirabilis Isolated from Macerated Diabetic Foot Ulcer

et al. 2021

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Diabetic foot ulcers are recognized to be a severe complication of diabetes, increasing the risk of amputation and death. The bacterial infection of Diabetic foot ulcers with virulent and resistant bacteria as Proteus mirabilis greatly worsens the wound and may not be treated with conventional therapeutics. Developing new approaches to target bacterial virulence can be helpful to conquer such infections. In the current work, we evaluated the anti-virulence activities of the widely used antibacterial metronidazole. The minimum inhibitory concentrations (MIC) and minimum biofilm eradication concentrations (MEBC) were determined for selected antibiotics which P. mirabilis was resistant to them in the presence and absence of metronidazole in sub-MIC. The effect of metronidazole in sub-MIC on P. mirabilis virulence factors as production of exoenzymes, motilities, adhesion and biofilm formation, were evaluated. Furthermore, molecular docking of metronidazole into P. mirabilis adhesion and essential quorum sensing (QS) proteins, was performed. The results revealed a significant ability of metronidazole to in-vitro inhibit P. mirabilis virulence factors and antagonize its essential proteins. Moreover, metronidazole markedly decreased the MICs and MBECs of tested antibiotics. Conclusively, metronidazole in sub-MIC is a plausible anti-virulence and anti-QS agent that can be combined to other antibiotics as anti-virulence adjuvant to defeat aggressive infections.

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Section: Mics and Mbecs Of Tested Antibiotics In Precence Of Metronidazole In Sub-micmentioning

confidence: 99%

Not Only Antimicrobial: Metronidazole Mitigates the Virulence of Proteus mirabilis Isolated from Macerated Diabetic Foot Ulcer

et al. 2021

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“…The QS system in S. marcescens' SmaI/SmaR communication system depends on secretion of autoinducers termed homoserine lactones (HSLs). QS orchestrates motility, biofilm formation, production of hydrolytic enzymes, and other virulence factors as lipase, protease, hemolysin, and chitinase [6,[44][45][46][47].…”

Section: Discussionmentioning

confidence: 99%

Xylitol Inhibits Growth and Blocks Virulence in Serratia marcescens

et al. 2021

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Serratia marcescens is an opportunistic nosocomial pathogen and causes wound and burn infections. It shows high resistance to antibiotics and its pathogenicity is mediated by an arsenal of virulence factors. Another therapeutic option to such infections is targeting quorum sensing (QS), which controls the expression of different S. marcescens virulence factors. Prevention of QS can deprive S. marcescens from its bacterial virulence without applying stress on the bacterial growth and facilitates the eradication of the bacteria by immunity. The objective of the current study is to explore the antimicrobial and antivirulence activities of xylitol against S. marcescens. Xylitol could inhibit the growth of S. marcescens. Sub-inhibitory concentrations of xylitol could inhibit biofilm formation, reduce prodigiosin production, and completely block protease activity. Moreover, xylitol decreased swimming motility, swarming motility and increased the sensitivity to hydrogen peroxide. The expression of rsmA, pigP, flhC, flhD fimA, fimC, shlA bsmB, and rssB genes that regulate virulence factor production was significantly downregulated by xylitol. In silico study showed that xylitol could bind with the SmaR receptor by hydrophobic interaction and hydrogen bonding, and interfere with the binding of the natural ligand with SmaR receptor. An in vivo mice survival test confirmed the ability of xylitol to protect mice against the virulence of S. marcescens. In conclusion, xylitol is a growth and virulence inhibitor in S. marcescens and can be employed for the treatment of S. marcescens wound and burn infections.

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“…The quorum-sensing (QS) system plays the most crucial roles in orchestrating the expression of virulence factors associated with numerous pathogenic phenotypes such as bacterial adherence and biofilm formation [ 13 , 22 , 25 , 35 ]. Inhibition of QS is an attractive approach and is considered a novel solution to the problem of antibiotic resistance development [ 24 , 26 ].…”

Section: Discussionmentioning

confidence: 99%

“…The allopurinol’s ability to inhibit biofilm formation was assessed as described before [ 13 , 19 ]. A bacterial suspension of PAO1 with a cell density of 1 × 10 6 CFU/mL was prepared in TSB from fresh overnight cultures.…”

Section: Methodsmentioning

confidence: 99%

“…Quorum-sensing (QS) systems are common in bacterial pathogens, including P. aeruginosa [ 11 , 12 , 13 ], that employ them to regulate bacterial virulence. P. aeruginosa virulence is controlled by three QS systems, two of which are LuxI/LuxR types and one which is a non-LuxI/LuxR type, namely, the Pseudomonas quinolone signal (PQS) system [ 7 ].…”

Section: Introductionmentioning

confidence: 99%

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A Novel Use of Allopurinol as A Quorum-Sensing Inhibitor in Pseudomonas aeruginosa

et al. 2021

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Pseudomonas aeruginosa can cause a variety of healthcare-associated infections by its arsenal of virulence factors. Virulence factor production is largely controlled by the cell-to-cell communication system termed quorum sensing (QS). Targeting QS may be a good approach to inhibit the production of virulence factors and attenuate pathogenicity without exerting selective stress on bacterial growth. This will greatly reduce the emergence of resistant mutants. In this work, we investigated the anti-virulence and anti-QS activities of the FDA-approved drug allopurinol against the P. aeruginosa PAO1 strain. Allopurinol at 200 µg/mL (1/10 MIC) significantly decreased the production of the QS-controlled Chromobacterium violaceum CV026 violet pigment violacein and other P. aeruginosa QS-controlled virulence factors phenotypically. Furthermore, allopurinol reduced the infiltration of P. aeruginosa and leucocytes and diminished the congestion in the liver and kidney tissues of infected mice. In silico study showed that allopurinol could compete with the autoinducers on binding to the receptors LasR and RhlR by hydrogen bonding. On the molecular level, qRT-PCR proved that allopurinol showed a significant downregulating effect on all tested QS-encoding genes that regulate virulence factor production. In summary, allopurinol is a promising QS inhibitor that may be useful in the future treatment of P. aeruginosa infection.

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Evaluation of the role of SsaV Salmonella pathogenicity island-2 dependent type III secretion system components on the virulence behavior of Salmonella enterica serovar Typhimurium

Cited by 34 publications

References 26 publications

Not Only Antimicrobial: Metronidazole Mitigates the Virulence of Proteus mirabilis Isolated from Macerated Diabetic Foot Ulcer

Not Only Antimicrobial: Metronidazole Mitigates the Virulence of Proteus mirabilis Isolated from Macerated Diabetic Foot Ulcer

Xylitol Inhibits Growth and Blocks Virulence in Serratia marcescens

A Novel Use of Allopurinol as A Quorum-Sensing Inhibitor in Pseudomonas aeruginosa

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