2-tert-Butyl-1,4-benzoquinone, a food additive oxidant, reduces virulence factors of Chromobacterium violaceum

Xu, Kai-Zhong; Tan, Xiaojuan; Chang, Zengyan; Li, Junjian; Jia, Ai‐Qun

doi:10.1016/j.lwt.2022.113569

Cited by 10 publications

(10 citation statements)

References 46 publications

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“…Our previous study showed that TBQ possesses a QS-inhibitory effect on the pathogenic bacterium C. violaceum ATCC 12472. In addition, the combination of TBQ (50 μg/mL) and ciprofloxacin (sub-MIC, 0.2 μg/mL) synergistically inhibited biofilm formation by 73.27% ( 16 ). Therefore, the effects of ZnO-NPs (25 μg/mL) on the production of virulence factors and the inhibition of biofilm formation by C. violaceum ATCC 12472 were investigated in the present study at sub-MICs without inhibiting planktonic growth.…”

Section: Discussionmentioning

confidence: 99%

“…The combination of a QS inhibitor and a conventional antibiotic is known as a promising approach for eradicating preformed biofilms and decreasing the magnitude of the infection ( 16 ). Alternatively, we suggest that the combination of TBQ and ZnO-NPs could reduce the use of antibiotics and, consequently, attenuate the risk of antibiotic resistance.…”

Section: Discussionmentioning

confidence: 99%

“…Our previous studies indicated that 2- tert -butyl-1,4-benzoquinone (TBQ) acts as a QSI against C. violaceum ATCC 12472 ( 16 ). Here, the aim of this study is to investigate if the combination of ZnO-NPs with TBQ (ZnO-TBQ) results in a synergistic effect on the inhibition of virulence factors and biofilm formation.…”

Section: Introductionmentioning

confidence: 99%

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Combination of 2- tert -Butyl-1,4-Benzoquinone (TBQ) and ZnO Nanoparticles, a New Strategy To Inhibit Biofilm Formation and Virulence Factors of Chromobacterium violaceum

Liu

Chang

et al. 2023

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The combination of ZnO-NPs and TBQ (ZnO-TBQ) can compete with the inducer N -decanoyl-homoserine lactone (C 10 -HSL) by binding to CviR and downregulate genes related to the CviI/CviR system to interrupt the QS system of C. violaceum ATCC 12472. The downstream genes responding to cviR were also downregulated so that virulence factors and biofilm formation were inhibited.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Combination of 2- tert -Butyl-1,4-Benzoquinone (TBQ) and ZnO Nanoparticles, a New Strategy To Inhibit Biofilm Formation and Virulence Factors of Chromobacterium violaceum

Liu

Chang

et al. 2023

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“…200 μL suspension was added to 96-well microporous plate (polystyrene). Biofilm production was analyzed by incubating 96-well cell culture plates with 0.1% crystal violet solution (Merck KGaA, Germany) for 15 minutes as previously described ( Xu et al., 2022 ). The stained biofilm was recorded with a multifunctional microplate detector after dissolving 200μl of 33% acetic acid measured by OD 590 nm.…”

Section: Methodsmentioning

confidence: 99%

The temperature-dependent expression of type II secretion system controls extracellular product secretion and virulence in mesophilic Aeromonas salmonida SRW-OG1

Chen

Cai

et al. 2022

Front. Cell. Infect. Microbiol.

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Aeromonas salmonicida is a typical cold water bacterial pathogen that causes furunculosis in many freshwater and marine fish species worldwide. In our previous study, the pathogenic A. salmonicida (SRW-OG1) was isolated from a warm water fish, Epinephelus coioides was genomics and transcriptomics analyzed. Type II secretion system was found in the genome of A. salmonicida SRW-OG1, while the expressions of tatA, tatB, and tatC were significantly affected by temperature stress. Also, sequence alignment analysis, homology analysis and protein secondary structure function analysis showed that tatA, tatB, and tatC were highly conservative, indicating their biological significance. In this study, by constructing the mutants of tatA, tatB, and tatC, we investigated the mechanisms underlying temperature-dependent virulence regulation in mesophilic A. salmonida SRW-OG1. According to our results, tatA, tatB, and tatC mutants presented a distinct reduction in adhesion, hemolysis, biofilm formation and motility. Compared to wild-type strain, inhibition of the expression of tatA, tatB, and tatC resulted in a decrease in biofilm formation by about 23.66%, 19.63% and 40.13%, and a decrease in adhesion ability by approximately 77.69%, 80.41% and 62.14% compared with that of the wild-type strain. Furthermore, tatA, tatB, and tatC mutants also showed evidently reduced extracellular enzymatic activities, including amylase, protease, lipase, hemolysis and lecithinase. The genes affecting amylase, protease, lipase, hemolysis, and lecithinase of A. salmonicida SRW-OG1 were identified as cyoE, ahhh1, lipA, lipB, pulA, HED66_RS01350, HED66_RS19960, aspA, fabD, and gpsA, which were notably affected by temperature stress and mutant of tatA, tatB, and tatC. All above, tatA, tatB and tatC regulate the virulence of A. salmonicida SRW-OG1 by affecting biofilm formation, adhesion, and enzymatic activity of extracellular products, and are simultaneously engaged in temperature-dependent pathogenicity.

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“…The ability to form biofilms by 37 SDSD isolates from bovine clinical mastitis obtained between 2011 and 2013 [collection II, ( Alves-Barroco et al., 2021 )] was evaluated on polystyrene and glass surface (borosilicate test tubes) according to previously described protocols ( Genteluci et al., 2015 ; Alves-Barroco et al., 2019 ; Xu et al., 2022 ). For a comparative analysis, 18 SDSD isolates from bovine clinical mastitis (collection I) ( Rato et al., 2013 ; Alves-Barroco et al., 2019 ), obtained between 2002 and 2003, were included in the study.…”

Section: Methodsmentioning

confidence: 99%

Assessing in vivo and in vitro biofilm development by Streptococcus dysgalactiae subsp. dysgalactiae using a murine model of catheter-associated biofilm and human keratinocyte cell

Alves-Barroco

Botelho²,

Américo³

et al. 2022

Front. Cell. Infect. Microbiol.

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Streptococcus dysgalactiae subsp. dysgalactiae (SDSD) is an important agent of bovine mastitis. This infection causes an inflammatory reaction in udder tissue, being the most important disease-causing significant impact on the dairy industry. Therefore, it leads to an increase in dairy farming to meet commercial demands. As a result, there is a major impact on both the dairy industry and the environment including global warming. Recurrent mastitis is often attributed to the development of bacterial biofilms, which promote survival of sessile cells in hostile environments, and resistance to the immune system defense and antimicrobial therapy. Recently, we described the in vitro biofilm development on abiotic surfaces by bovine SDSD. In that work we integrated microbiology, imaging, and computational methods to evaluate the biofilm production capability of SDSD isolates on abiotic surfaces. Additionally, we reported that bovine SDSD can adhere and internalize human cells, including human epidermal keratinocyte (HEK) cells. We showed that the adherence and internalization rates of bovine SDSD isolates in HEK cells are higher than those of a SDSD DB49998-05 isolated from humans. In vivo, bovine SDSD can cause invasive infections leading to zebrafish morbidity and mortality. In the present work, we investigated for the first time the capability of bovine SDSD to develop biofilm in vivo using a murine animal model and ex-vivo on human HEK cells. Bovine SDSD isolates were selected based on their ability to form weak, moderate, or strong biofilms on glass surfaces. Our results showed that SDSD isolates displayed an increased ability to form biofilms on the surface of catheters implanted in mice when compared to in vitro biofilm formation on abiotic surface. A greater ability to form biofilm in vitro after animal passage was observed for the VSD45 isolate, but not for the other isolates tested. Besides that, in vitro scanning electron microscopy demonstrated that SDSD biofilm development was visible after 4 hours of SDSD adhesion to HEK cells. Cell viability tests showed an important reduction in the number of HEK cells after the formation of SDSD biofilms. In this study, the expression of genes encoding BrpA-like (biofilm regulatory protein), FbpA (fibronectin-binding protein A), HtrA (serine protease), and SagA (streptolysin S precursor) was higher for biofilm grown in vivo than in vitro, suggesting a potential role for these virulence determinants in the biofilm-development, host colonization, and SDSD infections. Taken together, these results demonstrate that SDSD can develop biofilms in vivo and on the surface of HEK cells causing important cellular damages. As SDSD infections are considered zoonotic diseases, our data contribute to a better understanding of the role of biofilm accumulation during SDSD colonization and pathogenesis not only in bovine mastitis, but they also shed some lights on the mechanisms of prosthesis-associated infection and cellulitis caused by SDSD in humans, as well.

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2-tert-Butyl-1,4-benzoquinone, a food additive oxidant, reduces virulence factors of Chromobacterium violaceum

Cited by 10 publications

References 46 publications

Combination of 2- tert -Butyl-1,4-Benzoquinone (TBQ) and ZnO Nanoparticles, a New Strategy To Inhibit Biofilm Formation and Virulence Factors of Chromobacterium violaceum

Combination of 2- tert -Butyl-1,4-Benzoquinone (TBQ) and ZnO Nanoparticles, a New Strategy To Inhibit Biofilm Formation and Virulence Factors of Chromobacterium violaceum

The temperature-dependent expression of type II secretion system controls extracellular product secretion and virulence in mesophilic Aeromonas salmonida SRW-OG1

Assessing in vivo and in vitro biofilm development by Streptococcus dysgalactiae subsp. dysgalactiae using a murine model of catheter-associated biofilm and human keratinocyte cell

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