Dataset Information

1,8-Cineole inhibits biofilm formation and bacterial pathogenicity by suppressing luxS gene expression in Escherichia coli.

ABSTRACT: In recent years, with frequent reports of multi-drug resistant strains, bacteria antibiotic resistance has become an increasingly serious health problem worldwide. One of the most promising ways for combating bacterial infections and antibiotic resistance is development of quorum-sensing (QS) interfering drugs. In this study, the results show that 1,8-cineole inhibited the expression of QS as well as the virulence genes in Escherichia coli O101 (E. coli O101) with a 65% inhibition rate against luxS gene. Therefore, we hypothesized that 1,8-cineole may inhibit the biofilm formation and reduce the pathogenicity of E. coli O101 by inhibiting the expression of luxS gene. To confirm our hypotheses, a luxS gene deleted E. coli O101 was constructed. The results show that the biofilm formation, motility, structure and pathogenicity of E. coli O101 were significantly inhibited following deletion of the luxS gene. In addition, the transcript levels of QS and virulence genes of E. coli O101 were also significantly down-regulated. Interestingly, 1,8-cineole no longer had a significant inhibitory effect on the related phenotype and gene expression of E. coli O101 without luxS gene. In conclusion, the results show that 1,8-cineole can affect bacterial biofilm formation and pathogenicity by suppressing the expression of luxS gene in E. coli O101, which could provide a new perspective for dealing with the biofilm problem of pathogenic bacteria.

SUBMITTER: Wang Y

PROVIDER: S-EPMC9624193 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature

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1,8-Cineole inhibits biofilm formation and bacterial pathogenicity by suppressing luxS gene expression in Escherichia coli.

Wang Yiming Y Zhang Yu Y Song Xu X Fang Chunlin C Xing Rui R Liu Lu L Zhao Xinghong X Zou Yuanfeng Y Li Lixia L Jia Renyong R Ye Gang G Shi Fei F Zhou Xun X Zhang Yingying Y Wan Hongping H Wei Qin Q Yin Zhongqiong Z

Frontiers in pharmacology 20221014

In recent years, with frequent reports of multi-drug resistant strains, bacteria antibiotic resistance has become an increasingly serious health problem worldwide. One of the most promising ways for combating bacterial infections and antibiotic resistance is development of quorum-sensing (QS) interfering drugs. In this study, the results show that 1,8-cineole inhibited the expression of QS as well as the virulence genes in Escherichia coli O101 (E. coli O101) with a 65% inhi ...[more]

PMID: 36330093

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Project description:BackgroundAs a quorum sensing system, LuxS/AI-2 is closely associated with bacterial growth, biofilm formation, and virulence. As yet, it is not known how the luxS is associated with a diverse array of physiological activities in non- carbapenemase producing carbapenem resistant Escherichia coli (non-CP-CREC). The purpose of this study is to explore the characterization of AI-2/LuxS quorum sensing system in antibiotic resistance, pathogenicity of non-CP-CREC.MethodsA total of five non-CP-CREC isolates that did not have ompC and ompF deletions were collected from various clinical samples from January 2021 to December 2023. RT-qPCR was used to detect genes expression of luxS, acrA, acrB, tolC, mdtB, mdtC, mdtE, mdtF, ompA, ompX, IL-8, IL-6, and TNF-α. Homologous recombination was used to create the luxS knockout strain. Transcriptome sequencing was utilized to analyze gene expression changes before and after the luxS knockout. Biofilm formation was detected using crystal violet staining. Antimicrobial susceptibility test was used to determine drug resistance. Bacterial growth curves were used to detect the influence of the luxS on bacterial growth. A cell infection assay was used to detect the impact of the luxS on bacterial adhesion and the inflammatory response it induces.ResultsOur results indicated that the expression of the luxS was significantly elevated in non-CP-CREC strains compared to the carbapenem antibiotics sensitive E. coli (CSEC), with CREC229 exhibiting the most pronounced difference. Consequently, CREC229 was chosen for the development of the luxS knockout strain (CREC229△luxS). The deletion of the luxS did not impact the growth of non-CP-CREC. RNA sequencing analysis revealed that 82 genes were differentially expressed, with notable alterations observed in genes associated with biofilm formation regulation and outer membrane proteins in the ΔluxS strain. Our transcriptomic results show that the expression of bssS associated with biofilm formation is significantly reduced in the ΔluxS strain, which in turn reduces its capacity for biofilm formation. In addition, the luxS deletion increased the expression of adhesion-related genes, such as ompA and ompX, enhanced HCT-8 adherence to CREC229, and promoted the secretion of the inflammatory cytokine IL-6. In terms of bacterial resistance, the deletion of luxS increased the sensitivity of non-CP-CRECs to aminoglycoside antibiotics.ConclusionsLuxS/AI-2 quorum sensing systems can alter pathogenicity and resistance in several ways.

Project description:Uropathogenic Escherichia coli (UPEC) is a frequent cause of catheter-associated urinary tract infection (CAUTI). Biocides have been incorporated into catheter coatings to inhibit bacterial colonization while, ideally, exhibiting low cytotoxicity and mitigating the selection of resistant bacterial populations. We compared the effects of long-term biocide exposure on susceptibility, biofilm formation, and relative pathogenicity in eight UPEC isolates. MICs, minimum bactericidal concentrations (MBCs), minimum biofilm eradication concentrations (MBECs), and antibiotic susceptibilities were determined before and after long-term exposure to triclosan, polyhexamethylene biguanide (PHMB), benzalkonium chloride (BAC), and silver nitrate. Biofilm formation was quantified using a crystal violet assay, and relative pathogenicity was assessed via a Galleria mellonella waxworm model. Cytotoxicity and the resulting biocompatibility index values were determined by use of an L929 murine fibroblast cell line. Biocide exposure resulted in multiple decreases in biocide susceptibility in planktonic and biofilm-associated UPEC. Triclosan exposure induced the largest frequency and magnitude of susceptibility decreases at the MIC, MBC, and MBEC, which correlated with an increase in biofilm biomass in all isolates. Induction of antibiotic cross-resistance occurred in 6/84 possible combinations of bacteria, biocide, and antibiotic. Relative pathogenicity significantly decreased after triclosan exposure (5/8 isolates), increased after silver nitrate exposure (2/8 isolates), and varied between isolates for PHMB and BAC. The biocompatibility index ranked the antiseptic potential as PHMB > triclosan > BAC > silver nitrate. Biocide exposure in UPEC may lead to reductions in biocide and antibiotic susceptibility, changes in biofilm formation, and alterations in relative pathogenicity. These data indicate the multiple consequences of biocide adaptation that should be considered when selecting an anti-infective catheter-coating agent.

Dataset Information

1,8-Cineole inhibits biofilm formation and bacterial pathogenicity by suppressing luxS gene expression in Escherichia coli.

Publications

1,8-Cineole inhibits biofilm formation and bacterial pathogenicity by suppressing <i>luxS</i> gene expression in <i>Escherichia coli</i>.

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