Effect and mechanism of quorum sensing on horizontal transfer of multidrug plasmid RP4 in BAC biofilm. - Related Documents




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896101.0000Effect and mechanism of quorum sensing on horizontal transfer of multidrug plasmid RP4 in BAC biofilm. The widespread emergence of antibiotic resistance genes (ARGs) in drinking water systems endangers human health, and may be exacerbated by their horizontal gene transfer (HGT) among microbiota. In our previous study, Quorum sensing (QS) molecules produced by bacteria from biological activated carbon (BAC) biofilms were demonstrated to influence the transfer efficiency of a model conjugative plasmid, here RP4. In this study, we further explored the effect and mechanism of QS on conjugation transfer. The results revealed that Acyl-homoserine lactones producing (AHL-producing) bacteria isolated from BAC biofilm play a role in the propagation of ARGs. We selected several quorum sensing inhibitors (QSIs) to study their effects on AHL-producing bacteria, including the formation of biofilm and the regulating effect on conjugation transfer. In addition, the possible molecular mechanisms for AHLs that promote conjugative transfer were attributable to enhancing the mRNA expression, which involved altered expressions of conjugation-related genes. We also found that QSIs could inhibit conjugative transfer by downregulating the conjugation-relevant genes. We believe that this is the first insightful exploration of the mechanism by which AHLs will facilitate and QSIs will inhibit the conjugative transfer of ARGs. These results provide creative insight into ARG pollution control that involves blocking QS during BAC treatment in drinking water systems.202031493577
897510.9998Targeting bacterial biofilm-related genes with nanoparticle-based strategies. Persistent infection caused by biofilm is an urgent in medicine that should be tackled by new alternative strategies. Low efficiency of classical treatments and antibiotic resistance are the main concerns of the persistent infection due to biofilm formation which increases the risk of morbidity and mortality. The gene expression patterns in biofilm cells differed from those in planktonic cells. One of the promising approaches against biofilms is nanoparticle (NP)-based therapy in which NPs with multiple mechanisms hinder the resistance of bacterial cells in planktonic or biofilm forms. For instance, NPs such as silver (Ag), zinc oxide (ZnO), titanium dioxide (TiO(2)), copper oxide (Cu), and iron oxide (Fe(3)O(4)) through the different strategies interfere with gene expression of bacteria associated with biofilm. The NPs can penetrate into the biofilm structure and affect the expression of efflux pump, quorum-sensing, and adhesion-related genes, which lead to inhibit the biofilm formation or development. Therefore, understanding and targeting of the genes and molecular basis of bacterial biofilm by NPs point to therapeutic targets that make possible control of biofilm infections. In parallel, the possible impact of NPs on the environment and their cytotoxicity should be avoided through controlled exposure and safety assessments. This study focuses on the biofilm-related genes that are potential targets for the inhibition of bacterial biofilms with highly effective NPs, especially metal or metal oxide NPs.202438841057
428620.9997Disinfectant resistance in bacteria: Mechanisms, spread, and resolution strategies. Disinfectants are widely acknowledged for removing microorganisms from the surface of the objects and transmission media. However, the emergence of disinfectant resistance has become a severe threat to the safety of life and health and the rational allocation of resources due to the reduced disinfectant effectiveness. The horizontal gene transfer (HGT) of disinfectant resistance genes has also expanded the resistant flora, making the situation worse. This review focused on the resistance mechanisms of disinfectant resistant bacteria on biofilms, cell membrane permeability, efflux pumps, degradable enzymes, and disinfectant targets. Efflux can be the fastest and most effective resistance mechanism for bacteria to respond to stress. The qac genes, located on some plasmids which can transmit resistance through conjugative transfer, are the most commonly reported in the study of disinfectant resistance genes. Whether the qac genes can be transferred through transformation or transduction is still unclear. Studying the factors affecting the resistance of bacteria to disinfectants can find breakthrough methods to more adequately deal with the problem of reduced disinfectant effectiveness. It has been confirmed that the interaction of probiotics and bacteria or the addition of 4-oxazolidinone can inhibit the formation of biofilms. Chemicals such as eugenol and indole derivatives can increase bacterial sensitivity by reducing the expression of efflux pumps. The role of these findings in anti-disinfectant resistance has proved invaluable.202133617866
963430.9997New perspectives on bacterial chlorine resistance: Phages encoding chlorine resistance genes improve bacterial adaptation. Bacterial resistance to chlorine disinfectant reduces its effectiveness in killing pathogenic bacteria and poses a severe threat to environmental and health safety. The interaction between bacteria and phages is the most frequent biological activity in Earth's biosphere, but little is known about what role and mechanism phages play in the resistance of bacterial communities to chlorine disinfectants. Here, we investigated the changes in the abundance, activity and function of the bacterial-phage community under the effect of chlorine disinfectants in a 92-day running anaerobic-anoxic-oxic system, using metagenomics and metatranscriptomics sequencing. We found that transcriptional activities of both bacteria and phage are highly sensitive to chlorine disinfectants, although their relative abundance was not obviously altered. The increase in both phage diversity and the ratio of temperate to lytic phages' average activity indicated phages, especially temperate, could play a crucial role in the response to chlorine disinfectants. Interestingly, the phages that carry chlorine resistance genes (CRGs) were the drivers of the phage and microbial community when chlorine disinfectants were present, but they followed the dynamics of community in the absence of chlorine disinfectants. Based on the association bipartite network, we further found that phages directly mediated the horizontal transfer of CRGs among bacteria, facilitating the spread of CRGs in the bacterial community. Moreover, the 4 CRGs related to cell wall repair, redox balance regulation, and efflux pumps that were carried by the phages but lacking in the hosts suggest the potential compensatory effects of the phage for the chlorine resistance of their hosts. Our findings reveal the important role of phages in improving the resistance of bacterial communities to chlorine disinfectants, providing a new perspective on the co-evolution of phages and bacteria to adapt to environments.202540245807
963840.9997Response of microbial antibiotic resistance to pesticides: An emerging health threat. The spread of microbial antibiotic resistance has seriously threatened public health globally. Non-antibiotic stressors have significantly contributed to the evolution of bacterial antibiotic resistance. Although numerous studies have been conducted on the potential risk of pesticide pollution for bacterial antibiotic resistance, a systematic review of these concerns is still lacking. In the present study, we elaborate the mechanism underlying the effects of pesticides on bacterial antibiotic resistance acquisition as well as the propagation of antimicrobial resistance. Pesticide stress enhanced the acquisition of antibiotic resistance in bacteria via various mechanisms, including the activation of efflux pumps, inhibition of outer membrane pores for resistance to antibiotics, and gene mutation induction. Horizontal gene transfer is a major mechanism whereby pesticides influence the transmission of antibiotic resistance genes (ARGs) in bacteria. Pesticides promoted the conjugation transfer of ARGs by increasing cell membrane permeability and increased the proportion of bacterial mobile gene elements, which facilitate the spread of ARGs. This review can improve our understanding regarding the pesticide-induced generation and spread of ARGs and antibiotic resistant bacteria. Moreover, it can be applied to reduce the ecological risks of ARGs in the future.202235977623
898150.9997Response mechanisms of different antibiotic-resistant bacteria with different resistance action targets to the stress from photocatalytic oxidation. The stress response of antibiotic-resistant bacteria (ARB) and the spread of antibiotic resistance genes (ARGs) pose a serious threat to the aquatic environment and human beings. This study mainly explored the effect of the heterogeneous photocatalytic oxidation (UVA-TiO(2) system) on the stress response mechanism of ARB with different antibiotic resistance action targets, including the cell wall, proteins, DNA, RNA, folate and the cell membrane. Results indicate that the stress response mechanism of tetracycline- and sulfamethoxazole-resistant E. coli DH5α, which targets the synthesis of protein and folate, could rapidly induce global regulators by the overexpression of relative antibiotic resistance action target genes. Different stress response systems were mediated via cross-protection mechanism, causing stronger tolerance to an adverse environment than other ARB. Moreover, the photocatalytic inactivation mechanism of bacterial cells and a graded response of cellular stress mechanism caused differences in the intensity of the stress mechanism of antibiotic resistance action targets. E. coli DH5α resistant to cefotaxime and polymyxin, targeting synthesis of the cell wall and cell membrane, respectively, could confer greater advantages to bacterial survival and higher conjugative transfer frequency than E. coli DH5α resistant to nalidixic acid and rifampicin, which target the synthesis of DNA and RNA, respectively. This new perspective provides detailed information on the practical application of photocatalytic oxidation for inactivating ARB and hampering the spreading of ARGs in the aquatic environment.202235453030
834560.9997Antibiotic Resistance via Bacterial Cell Shape-Shifting. Bacteria have evolved to develop multiple strategies for antibiotic resistance by effectively reducing intracellular antibiotic concentrations or antibiotic binding affinities, but the role of cell morphology in antibiotic resistance remains poorly understood. By analyzing cell morphological data for different bacterial species under antibiotic stress, we find that bacteria increase or decrease the cell surface-to-volume ratio depending on the antibiotic target. Using quantitative modeling, we show that by reducing the surface-to-volume ratio, bacteria can effectively reduce the intracellular antibiotic concentration by decreasing antibiotic influx. The model further predicts that bacteria can increase the surface-to-volume ratio to induce the dilution of membrane-targeting antibiotics, in agreement with experimental data. Using a whole-cell model for the regulation of cell shape and growth by antibiotics, we predict shape transformations that bacteria can utilize to increase their fitness in the presence of antibiotics. We conclude by discussing additional pathways for antibiotic resistance that may act in synergy with shape-induced resistance.202235616332
834470.9997Role of environmental stresses in elevating resistance mutations in bacteria: Phenomena and mechanisms. Mutations are an important origin of antibiotic resistance in bacteria. While there is increasing evidence showing promoted resistance mutations by environmental stresses, no retrospective research has yet been conducted on this phenomenon and its mechanisms. Herein, we summarized the phenomena of stress-elevated resistance mutations in bacteria, generalized the regulatory mechanisms and discussed the environmental and human health implications. It is shown that both chemical pollutants, such as antibiotics and other pharmaceuticals, biocides, metals, nanoparticles and disinfection byproducts, and non-chemical stressors, such as ultraviolet radiation, electrical stimulation and starvation, are capable of elevating resistance mutations in bacteria. Notably, resistance mutations are more likely to occur under sublethal or subinhibitory levels of these stresses, suggesting a considerable environmental concern. Further, mechanisms for stress-induced mutations are summarized in several points, namely oxidative stress, SOS response, DNA replication and repair systems, RpoS regulon and biofilm formation, all of which are readily provoked by common environmental stresses. Given bacteria in the environment are confronted with a variety of unfavorable conditions, we propose that the stress-elevated resistance mutations are a universal phenomenon in the environment and represent a nonnegligible risk factor for ecosystems and human health. The present review identifies a need for taking into account the pollutants' ability to elevate resistance mutations when assessing their environmental and human health risks and highlights the necessity of including resistance mutations as a target to prevent antibiotic resistance evolution.202235691443
896280.9997A Dietary Source of High Level of Fluoroquinolone Tolerance in mcr-Carrying Gram-Negative Bacteria. The emergence of antibiotic tolerance, characterized by the prolonged survival of bacteria following antibiotic exposure, in natural bacterial populations, especially in pathogens carrying antibiotic resistance genes, has been an increasing threat to public health. However, the major causes contributing to the formation of antibiotic tolerance and underlying molecular mechanisms are yet poorly understood. Herein, we show that potassium sorbate (PS), a widely used food additive, triggers a high level of fluoroquinolone tolerance in bacteria carrying mobile colistin resistance gene mcr. Mechanistic studies demonstrate that PS treatment results in the accumulation of intracellular fumarate, which activates bacterial two-component system and decreases the expression level of outer membrane protein OmpF, thereby reducing the uptake of ciprofloxacin. In addition, the supplementation of PS inhibits aerobic respiration, reduces reactive oxygen species production and alleviates DNA damage caused by bactericidal antibiotics. Furthermore, we demonstrate that succinate, an intermediate product of the tricarboxylic acid cycle, overcomes PS-mediated ciprofloxacin tolerance. In multiple animal models, ciprofloxacin treatment displays failure outcomes in PS preadministrated animals, including comparable survival and bacterial loads with the vehicle group. Taken together, our works offer novel mechanistic insights into the development of antibiotic tolerance and uncover potential risks associated with PS use.202337808177
916290.9997Joint effects of antibiotics and quorum sensing inhibitors on resistance development in bacteria. Quorum sensing inhibitors (QSIs) are promising alternatives to antibiotics. While QSIs have great application potential in a variety of fields, their joint effects with antibiotics on bacteria, especially on antibiotic resistance mutations, remain largely unexplored. Herein, we report the joint effects of four commonly used antibiotics and two QSIs on bacterial growth and resistance mutations in E. coli. It was found that QSIs presented antagonistic or additive effects with antibiotics on bacterial growth, and more importantly, QSIs exhibited an attenuating effect on antibiotic-induced resistance mutations. Further analysis demonstrated that antibiotics might enhance resistance mutations by promoting the expressions of rpoS, lexA and recA, while QSIs attenuated the mutations by promoting the expressions of mutS and uvrD. The present research provides a comprehensive understanding of the joint effects of antibiotics and QSIs on bacteria, which may benefit the risk assessment of their combined exposure.202134060581
6774100.9997Both silver ions and silver nanoparticles facilitate the horizontal transfer of plasmid-mediated antibiotic resistance genes. Antibiotic resistance in bacteria is a growing threat to global human health. Horizontal gene transfer (HGT) of antibiotic resistance genes (ARGs) is recognized as the primary contributor to antibiotic resistance dissemination. Silver nanoparticles (AgNPs) are widely used in personal care products as antimicrobial agents. While heavy metals are known to induce antibiotic resistance in bacteria, it is not known whether AgNPs in the environment can stimulate the HGT of ARGs. Here, we report that both AgNPs and ionic silver Ag(+), at environmentally relevant and sub-lethal concentrations, facilitate the conjugative transfer of plasmid-borne ARGs across bacterial genera (from the donor Escherichia coli K-12 LE392 to the recipient Pseudomonas putida KT2440). The underlying mechanisms of the Ag(+)- or AgNPs-promoted HGT were unveiled by detecting oxidative stress and cell membrane permeability, combined with genome-wide RNA sequencing and proteomic analyses. It was found that both Ag(+) and AgNPs exposure induced various bacterial responses that included reactive oxygen species (ROS) generation, membrane damage and the SOS response. This study exposes the potential ecological risks of environmental levels of AgNPs and Ag(+) for promoting the spread of ARGs and highlights concerns regarding the management of nanoparticles and heavy metals.202031783256
8983110.9997Chlorine disinfectants promote microbial resistance in Pseudomonas sp. The substantial use of disinfectants has increased antibiotic resistance, thereby mediating serious ecological safety issues worldwide. Accumulating studies have reported the role of chlorine disinfectants in promoting disinfectant resistance. The present study sought to investigate the role of chlorine disinfectants in developing multiple resistance in Pseudomonas sp. isolated from the river through antioxidant enzyme measurement, global transcriptional analyses, Gene Ontology (GO), and the Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. The results demonstrated that 100 mg/L sodium hypochlorite could increase disinfectant resistance and antibiotic resistance. The SOS response (a conserved response to DNA damage) triggered by oxidative stress makes bacteria resistant to chlorine. An increase in antibiotic resistance could be attributed to a decreased membrane permeability, increased expression of MuxABC-OpmB efflux pump, beta-lactamase, and antioxidant enzymes. Additionally, KEGG enrichment analysis suggested that the differentially expressed genes were highly enriched in the metabolic pathways. In summary, the study results revealed the impact of chlorine disinfectants in promoting microbial disinfectant resistance and antibiotic resistance. This study will provide insight into disinfectant resistance mechanisms.202134010624
8982120.9997Ampicillin Exposure and Glutathione Deficiency Synergistically Promote Conjugative Transfer of Plasmid-Borne Antibiotic Resistance Genes. Plasmid-mediated conjugation is an important pathway for the spread of antibiotic resistance genes (ARGs), posing a significant risk to global public health. It has been reported that the conjugative transfer of ARGs could be enhanced by oxidative stress. Whether endogenous glutathione (GSH), a major non-protein thiol compound involved in cellular redox homeostasis, influences conjugative transfer is unknown. In this study, we show that the deletion of the GSH biosynthesis gene gshA and ampicillin exposure synergistically promoted the conjugative transfer of plasmid RP4 bearing multiple ARGs from the soil bacterium Enterobacter sp. CZ-1 to Escherichia coli S17-1λπ in co-culture experiments and to diverse soil bacteria belonging to eight phyla, including some potential human pathogens, in a soil incubation experiment. The deletion of gshA increased ROS generation and cell membrane permeability, and upregulated the expression of the genes involved in intracellular oxidative stress regulation, membrane permeability, plasmid replication, and the SOS response process, especially under ampicillin exposure. These results suggest that endogenous GSH is an important factor affecting the spread of plasmid-borne ARGs. Exposure to antibiotics and environmental stresses that cause a depletion of endogenous GSH in vivo are likely to increase the risk of ARG dissemination in the environment.202540346915
6772130.9997Disinfectants facilitate the transformation of exogenous antibiotic resistance genes via multiple pathways. The prevalence and spread of multidrug-resistant (MDR) bacteria pose a global challenge to public health. Natural transformation is one of the essential ways for horizontal transfer of antibiotic resistance genes (ARGs). Although disinfectants are frequently used during COVID-19, little is known about whether these disinfectants are associated with the transformation of plasmid-borne ARGs. In our study, we assessed the effect of some disinfectants on bacterial transformation using resistance plasmids as extracellular DNA and E. coli DH5α as the recipient bacteria. The results showed that these disinfectants at environmentally relevant concentrations, including benzalkonium bromide (BB), benzalkonium chloride (BC) and polyhexamethylene guanidine hydrochloride (PHMG), significantly enhanced the transformation of plasmid-encoded ARGs. Furthermore, we investigated the mechanisms underlying the promotive effect of disinfectants on transformation. We revealed that the addition of disinfectants significantly increased the membrane permeability and promoted membrane-related genes expression. Moreover, disinfectants led to the boosted bacterial respiration, ATP production and flagellum motility, as well as increased expression of bacterial secretion system-related genes. Together, our findings shed insights into the spread of ARGs through bacterial transformation and indicate potential risks associated with the widespread use of disinfectants.202336857920
9429140.9997Basic features of biofilms--why are they difficult therapeutic targets? The purpose of this paper is to review the basic features of biofilms associated with human infections and summarize why such biofilms are resistant to antimicrobial agents. The formation of most biofilms involves adherence of bacteria to a conditioned surface, growth and division of the attached bacteria, synthesis of a polymeric slime matrix, formation of a structured microbial community, and incorporation of other micro-organisms into the microbial mass. The transition of bacteria from free-floating (planktonic) to biofilm environments involves extensive up-regulation of genes associated with adherence. Micro-organisms in established biofilms engage in complex integrated activities involving activation and deactivation of genes that promote the survival of bacteria within the biofilm community. Mechanisms of the increased resistance of biofilm bacteria to antimicrobial agents may involve: (1) neutralization or consumption of the drug, (2) failure of the drug to completely penetrate the biofilm, (3) inability of the drug to affect metabolically inactive bacteria, and (4) presence of drug-resistant bacteria within biofilms.200416479852
6778150.9997Bisphenol S Promotes the Transfer of Antibiotic Resistance Genes via Transformation. The antibiotic resistance crisis has seriously jeopardized public health and human safety. As one of the ways of horizontal transfer, transformation enables bacteria to acquire exogenous genes naturally. Bisphenol compounds are now widely used in plastics, food, and beverage packaging, and have become a new environmental pollutant. However, their potential relationship with the spread of antibiotic resistance genes (ARGs) in the environment remains largely unexplored. In this study, we aimed to assess whether the ubiquitous bisphenol S (BPS) could promote the transformation of plasmid-borne ARGs. Using plasmid pUC19 carrying the ampicillin resistance gene as an extracellular ARG and model microorganism E. coli DH5α as the recipient, we established a transformation system. Transformation assays revealed that environmentally relevant concentrations of BPS (0.1-10 μg/mL) markedly enhanced the transformation frequency of plasmid-borne ARGs into E. coli DH5α up to 2.02-fold. Fluorescent probes and transcript-level analyses suggest that BPS stimulated increased reactive oxygen species (ROS) production, activated the SOS response, induced membrane damage, and increased membrane fluidity, which weakened the barrier for plasmid transfer, allowing foreign DNA to be more easily absorbed. Moreover, BPS stimulates ATP supply by activating the tricarboxylic acid (TCA) cycle, which promotes flagellar motility and expands the search for foreign DNA. Overall, these findings provide important insight into the role of bisphenol compounds in facilitating the horizontal spread of ARGs and emphasize the need to monitor the residues of these environmental contaminants.202439337307
8601160.9997Herbicide promotes the conjugative transfer of multi-resistance genes by facilitating cellular contact and plasmid transfer. The global dissemination of antibiotic resistance genes (ARGs), especially via plasmid-mediated horizontal transfer, is becoming a pervasive health threat. While our previous study found that herbicides can accelerate the horizontal gene transfer (HGT) of ARGs in soil bacteria, the underlying mechanisms by which herbicides promote the HGT of ARGs across and within bacterial genera are still unclear. Here, the underlying mechanism associated with herbicide-promoted HGT was analyzed by detecting intracellular reactive oxygen species (ROS) production, extracellular polymeric substance composition, cell membrane integrity and proton motive force combined with genome-wide RNA sequencing. Exposure to herbicides induced a series of the above bacterial responses to promote HGT except for the ROS response, including compact cell-to-cell contact by enhancing pilus-encoded gene expression and decreasing cell surface charge, increasing cell membrane permeability, and enhancing the proton motive force, providing additional power for DNA uptake. This study provides a mechanistic understanding of the risk of bacterial resistance spread promoted by herbicides, which elucidates a new perspective on nonantibiotic agrochemical acceleration of the HGT of ARGs.202234969463
9146170.9997Emergence of microbial resistance against nanoparticles: Mechanisms and strategies. Antimicrobial nanoparticles have gained the status of a new generation of drugs that can kill bacterial pathogens by multiple means; however, nanoparticle resistance acquired by some bacterial pathogens has evoked a cause of concern. Several reports suggested that bacteria can develop nanoparticles, specifically metal nanoparticle resistance, by mechanisms: nanoparticle transformation-induced oxidative stress, membrane alterations, reversible adaptive resistance, irreversible modifications to cell division, and a change in bacterial motility and resistance. Surface properties, concentration and aggregation of nanoparticles, biofilm forming and metal exclusion capacity, and R plasmid and flagellin synthesis by bacteria are crucial factors in the development of nanoparticle resistance in bacteria. Studies reported the resistance reversal by modifying the surface corona of nanoparticles or inhibiting flagellin production by bacterial pathogens. Furthermore, strict regulation regarding the use and disposal of nano-waste across the globe, the firm knowledge of microbe-nanoparticle interaction, and the regulated disposal of nanoparticles in soil and water is required to prevent microbes from developing nanoparticle resistance.202336778867
9430180.9997Mechanisms of antimicrobial resistance in biofilms. Most bacteria in nature exist in aggregated communities known as biofilms, and cells within a biofilm demonstrate major physiological changes compared to their planktonic counterparts. Biofilms are associated with many different types of infections which can have severe impacts on patients. Infections involving a biofilm component are often chronic and highly recalcitrant to antibiotic therapy as a result of intrinsic physical factors including extracellular matrix production, low growth rates, altered antibiotic target production and efficient exchange of resistance genes. This review describes the biofilm lifecycle, phenotypic characteristics of a biofilm, and contribution of matrix and persister cells to biofilms intrinsic tolerance to antimicrobials. We also describe how biofilms can evolve antibiotic resistance and transfer resistance genes within biofilms. Multispecies biofilms and the impacts of various interactions, including cooperation and competition, between species on tolerance to antimicrobials in polymicrobial biofilm communities are also discussed.202439364333
8960190.9997Pyraclostrobin induces multi-antibiotic resistance in Escherichia coli via quorum sensing: A new perspective. Antibiotic resistance seriously threatens to global public health, and non-antibiotic chemicals like pesticides can contribute to its development. Quorum sensing (QS) is an intercellular communication system that regulates group behavior and can potentially become a pathway for the development of antibiotic resistance. This study firstly discovered that exposure to pyraclostrobin at 0.5 mg/L activated QS, resulting in antibiotic resistance in Escherichia coli, with minimum inhibitory concentrations (MICs) increasing by up to 128-fold against tested antibiotics. Mechanistically, the high expression of the luxS gene induced by pyraclostrobin stress increased the level of the QS signal molecule (AI-2), leading to enhanced QS in antibiotic-resistant bacteria (ARB), thereby upregulating the expression of multidrug efflux pump genes (acrB and marA) and downregulating the expression of outer membrane porin genes (ompC and ompF). Meanwhile, using a QS inhibitor also increased the strains' antibiotic sensitivity. Additionally, pyraclostrobin exposure damaged cell membranes, induced oxidative stress, and caused gene mutations, further promoting multidrug resistance. Overall, the findings demonstrate that pyraclostrobin exposure can stimulate antibiotic resistance in Escherichia coli by activating QS and inducing gene mutations. Therefore, the rigorous application of fungicides is essential to retard the development of antibiotic resistance.202540544772