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789000.9913The control of red water occurrence and opportunistic pathogens risks in drinking water distribution systems: A review. Many problems in drinking water distribution systems (DWDSs) are caused by microbe, such as biofilm formation, biocorrosion and opportunistic pathogens growth. More iron release from corrosion scales may induce red water. Biofilm played great roles on the corrosion. The iron-oxidizing bacteria (IOB) promoted corrosion. However, when iron-reducing bacteria (IRB) and nitrate-reducing bacteria (NRB) became the main bacteria in biofilm, they could induce iron redox cycling in corrosion process. This process enhanced the precipitation of iron oxides and formation of more Fe(3)O(4) in corrosion scales, which inhibited corrosion effectively. Therefore, the IRB and NRB in the biofilm can reduce iron release and red water occurrence. Moreover, there are many opportunistic pathogens in biofilm of DWDSs. The opportunistic pathogens growth in DWDSs related to the bacterial community changes due to the effects of micropollutants. Micropollutants increased the number of bacteria with antibiotic resistance genes (ARGs). Furthermore, extracellular polymeric substances (EPS) production was increased by the antibiotic resistant bacteria, leading to greater bacterial aggregation and adsorption, increasing the chlorine-resistance capability, which was responsible for the enhancement of the particle-associated opportunistic pathogens in DWDSs. Moreover, O(3)-biological activated carbon filtration-UV-Cl(2) treatment could be used to control the iron release, red water occurrence and opportunistic pathogens growth in DWDSs.202134593198
833910.9912Dynamical model of antibiotic responses linking expression of resistance genes to metabolism explains emergence of heterogeneity during drug exposures. Antibiotic responses in bacteria are highly dynamic and heterogeneous, with sudden exposure of bacterial colonies to high drug doses resulting in the coexistence of recovered and arrested cells. The dynamics of the response is determined by regulatory circuits controlling the expression of resistance genes, which are in turn modulated by the drug's action on cell growth and metabolism. Despite advances in understanding gene regulation at the molecular level, we still lack a framework to describe how feedback mechanisms resulting from the interdependence between expression of resistance and cell metabolism can amplify naturally occurring noise and create heterogeneity at the population level. To understand how this interplay affects cell survival upon exposure, we constructed a mathematical model of the dynamics of antibiotic responses that links metabolism and regulation of gene expression, based on the tetracycline resistancetetoperon inE. coli. We use this model to interpret measurements of growth and expression of resistance in microfluidic experiments, both in single cells and in biofilms. We also implemented a stochastic model of the drug response, to show that exposure to high drug levels results in large variations of recovery times and heterogeneity at the population level. We show that stochasticity is important to determine how nutrient quality affects cell survival during exposure to high drug concentrations. A quantitative description of how microbes respond to antibiotics in dynamical environments is crucial to understand population-level behaviors such as biofilms and pathogenesis.202438412523
876620.9912Partitioning the Effects of Soil Legacy and Pathogen Exposure Determining Soil Suppressiveness via Induced Systemic Resistance. Beneficial host-associated bacteria can assist plant protection against pathogens. In particular, specific microbes are able to induce plant systemic resistance. However, it remains largely elusive which specific microbial taxa and functions trigger plant immune responses associated with disease suppression. Here, we experimentally studied this by setting up two independent microcosm experiments that differed in the time at which plants were exposed to the pathogen and the soil legacy (i.e., soils with historically suppressive or conducive). Overall, we found soil legacy effects to have a major influence on disease suppression irrespective of the time prior to pathogen exposure. Rhizosphere bacterial communities of tomato plants were significantly different between the two soils, with potential beneficial strains occurring at higher relative abundances in the suppressive soil. Root transcriptome analysis revealed the soil legacy to induce differences in gene expression, most importantly, genes involved in the pathway of phenylpropanoid biosynthesis. Last, we found genes in the phenylpropanoid biosynthesis pathway to correlate with specific microbial taxa, including Gp6, Actinomarinicola, Niastella, Phaeodactylibacter, Longimicrobium, Bythopirellula, Brevundimonas, Ferruginivarius, Kushneria, Methylomarinovum, Pseudolabrys, Sphingobium, Sphingomonas, and Alterococcus. Taken together, our study points to the potential regulation of plant systemic resistance by specific microbial taxa, and the importance of soil legacy on disease incidence and eliciting plant-defense mechanisms.202236365269
58930.9911Insulin Signaling and Insulin Resistance Facilitate Trained Immunity in Macrophages Through Metabolic and Epigenetic Changes. Adaptation of the innate immune system has been recently acknowledged, explaining sustained changes of innate immune responses. Such adaptation is termed trained immunity. Trained immunity is initiated by extracellular signals that trigger a cascade of events affecting cell metabolism and mediating chromatin changes on genes that control innate immune responses. Factors demonstrated to facilitate trained immunity are pathogenic signals (fungi, bacteria, viruses) as well non-pathogenic signals such as insulin, cytokines, adipokines or hormones. These signals initiate intracellular signaling cascades that include AKT kinases and mTOR as well as histone methylases and demethylases, resulting in metabolic changes and histone modifications. In the context of insulin resistance, AKT signaling is affected resulting in sustained activation of mTORC1 and enhanced glycolysis. In macrophages elevated glycolysis readily impacts responses to pathogens (bacteria, fungi) or danger signals (TLR-driven signals of tissue damage), partly explaining insulin resistance-related pathologies. Thus, macrophages lacking insulin signaling exhibit reduced responses to pathogens and altered metabolism, suggesting that insulin resistance is a state of trained immunity. Evidence from Insulin Receptor as well as IGF1Receptor deficient macrophages support the contribution of insulin signaling in macrophage responses. In addition, clinical evidence highlights altered macrophage responses to pathogens or metabolic products in patients with systemic insulin resistance, being in concert with cell culture and animal model studies. Herein, we review the current knowledge that supports the impact of insulin signaling and other insulin resistance related signals as modulators of trained immunity.201931244863
650340.9910The role of operating parameters and oxidative damage mechanisms of advanced chemical oxidation processes in the combat against antibiotic-resistant bacteria and resistance genes present in urban wastewater. An upsurge in the study of antibiotic resistance in the environment has been observed in the last decade. Nowadays, it is becoming increasingly clear that urban wastewater is a key source of antibiotic resistance determinants, i.e. antibiotic-resistant bacteria and antibiotic resistance genes (ARB&ARGs). Urban wastewater reuse has arisen as an important component of water resources management in the European Union and worldwide to address prolonged water scarcity issues. Especially, biological wastewater treatment processes (i.e. conventional activated sludge), which are widely applied in urban wastewater treatment plants, have been shown to provide an ideal environment for the evolution and spread of antibiotic resistance. The ability of advanced chemical oxidation processes (AOPs), e.g. light-driven oxidation in the presence of H(2)O(2), ozonation, homogeneous and heterogeneous photocatalysis, to inactivate ARB and remove ARGs in wastewater effluents has not been yet evaluated through a systematic and integrated approach. Consequently, this review seeks to provide an extensive and critical appraisal on the assessment of the efficiency of these processes in inactivating ARB and removing ARGs in wastewater effluents, based on recent available scientific literature. It tries to elucidate how the key operating conditions may affect the process efficiency, while pinpointing potential areas for further research and major knowledge gaps which need to be addressed. Also, this review aims at shedding light on the main oxidative damage pathways involved in the inactivation of ARB and removal of ARGs by these processes. In general, the lack and/or heterogeneity of the available scientific data, as well as the different methodological approaches applied in the various studies, make difficult the accurate evaluation of the efficiency of the processes applied. Besides the operating conditions, the variable behavior observed by the various examined genetic constituents of the microbial community, may be directed by the process distinct oxidative damage mechanisms in place during the application of each treatment technology. For example, it was shown in various studies that the majority of cellular damage by advanced chemical oxidation may be on cell wall and membrane structures of the targeted bacteria, leaving the internal components of the cells relatively intact/able to repair damage. As a result, further in-depth mechanistic studies are required, to establish the optimum operating conditions under which oxidative mechanisms target internal cell components such as genetic material and ribosomal structures more intensively, thus conferring permanent damage and/or death and preventing potential post-treatment re-growth.201829153875
648850.9910Inactivation of antibiotic-resistant bacteria and antibiotic-resistance genes in wastewater streams: Current challenges and future perspectives. The discovery of antibiotics, which was once regarded as a timely medical intervention now leaves a bitter aftertaste: antimicrobial resistance (AMR), due to the unregulated use of these compounds and the poor management receiving wastewaters before discharge into pristine environments or the recycling of such treated waters. Wastewater treatment plants (WWTPs) have been regarded a central sink for the mostly unmetabolized or partially metabolised antibiotics and is also pivotal to the incidence of antibiotic resistance bacteria (ARBs) and their resistance genes (ARGs), which consistently contribute to the global disease burden and deteriorating prophylaxis. In this regard, we highlighted WWTP-antibiotics consumption-ARBs-ARGs nexus, which might be critical to understanding the epidemiology of AMR and also guide the precise prevention and remediation of such occurrences. We also discovered the unsophistication of conventional WWTPs and treatment techniques for adequate treatment of antibiotics, ARBs and ARGs, due to their lack of compliance with environmental sustainability, then ultimately assessed the prospects of cold atmospheric plasma (CAP). Herein, we observed that CAP technologies not only has the capability to disinfect wastewater polluted with copious amounts of chemicals and biologicals, but also have a potential to augment bioelectricity generation, when integrated into bio electrochemical modules, which future WWTPs should be retrofitted to accommodate. Therefore, further research should be conducted to unveil more of the unknowns, which only a snippet has been highlighted in this study.202236733776
848960.9910Signaling molecules accelerate the transmission of antibiotic resistance genes under the stress of copper. Heavy metals can accelerate the dissemination of antibiotic resistance genes (ARGs) in aquatic environments by imposing environmental stresses. Signaling molecules play a role in bacterial communication and help bacteria adapt to environmental stresses. However, little is known whether the presence of signaling molecules has an effect on the spread of ARGs induced by heavy metals. In this study, we investigated how N-decanoyl-L-homoserine lactone (C10-HSL) affects copper-induced conjugative transfer of ARGs. We calculated the conjugative transfer frequency and measured reactive oxygen species (ROS) production, membrane permeability, and the expression of relevant genes. The results demonstrated that the addition of C10-HSL increased the conjugative transfer frequency of ARGs under copper ions (Cu(2+)) stress, showing a 7.2-fold increase under 0.5 μM Cu(2+) and 0.39 μM C10-HSL treatment compared to the control. This enhancement was associated with elevated intracellular ROS production and increased membrane permeability. The reduced conjugative transfer frequency under anaerobic conditions or with thiourea treatment supported the key role of ROS in this process. Furthermore, ROS overproduction triggered the SOS response, as evidenced by a 9-fold upregulation of recA expression. C10-HSL also modulated membrane-associated gene expression by upregulating outer membrane porins and downregulating efflux pump genes under Cu(2+)stress. This study provides a new insight into the spread of ARGs in aquatic environments.202540840413
898070.9910Omics analyses indicate sdhC/D act as hubs of early response of E. coli to antibiotics. In recent years, the phenomenon of microbial resistance has become increasingly serious. The generation of reactive oxygen species (ROS) during the bactericidal process of antibiotics has attracted great interest, but little research has been done on the generation of ROS in the early stage of antibiotic action. We confirmed the rapid production of ROS by flow cytometry and transmission electron microscopy (TEM). GO (Gene Ontology) and KEGG (Kyoto Encyclopedia of Genes and Genomes) enrichment analysis indicated that the oxidative phosphorylation pathway is the key pathway of ROS production. Protein-protein interaction (PPI) network results indicate that sdhC/D are key genes in the oxidative phosphorylation pathway. The overexpression of sdhC/D resulted in a lower survival rate than the control strain after antibiotic treatments, which might be due to excess ROS induced by sdhC/D overexpression. The production of superoxide anion in the overexpress strain was significantly higher than that in the control strain, which further verified the importance of sdhC/D in the ROS release of bacteria. Current results showed that bacteria produce large amounts of ROS in the early stage of gentamicin and ampicillin action, and the regulation patterns of genes in the key pathway were consistent. sdhC/D are key genes in the early ROS release process of bacteria. Our study provides a basis for the search of ROS-related enhancers of antimicrobial action.202235933647
833780.9909Dynamic Boolean modelling reveals the influence of energy supply on bacterial efflux pump expression. Antimicrobial resistance (AMR) is a global health issue. One key factor contributing to AMR is the ability of bacteria to export drugs through efflux pumps, which relies on the ATP-dependent expression and interaction of several controlling genes. Recent studies have shown that significant cell-to-cell ATP variability exists within clonal bacterial populations, but the contribution of intrinsic cell-to-cell ATP heterogeneity is generally overlooked in understanding efflux pumps. Here, we consider how ATP variability influences gene regulatory networks controlling expression of efflux pump genes in two bacterial species. We develop and apply a generalizable Boolean modelling framework, developed to incorporate the dependence of gene expression dynamics on available cellular energy supply. Theoretical results show that differences in energy availability can cause pronounced downstream heterogeneity in efflux gene expression. Cells with higher energy availability have a superior response to stressors. Furthermore, in the absence of stress, model bacteria develop heterogeneous pulses of efflux pump gene expression which contribute to a sustained sub-population of cells with increased efflux expression activity, potentially conferring a continuous pool of intrinsically resistant bacteria. This modelling approach thus reveals an important source of heterogeneity in cell responses to antimicrobials and sheds light on potentially targetable aspects of efflux pump-related antimicrobial resistance.202235078338
824090.9909β-glucan-induced disease resistance in plants: A review. Systemic acquired resistance (SAR) and induced systemic resistance (ISR) are caused by various factors, including both pathogenic and non-pathogenic ones. β-glucan primarily originates from bacteria and fungi, some species of these organisms work as biological agents in causing diseases. When β-glucan enters plants, it triggers the defense system, leading to various reactions such as the production of proteins related to pathogenicity and defense enzymes. By extracting β-glucan from disturbed microorganisms and using it as an inducing agent, plant diseases can be effectively controlled by activating the plant's defense system. β-glucan plays a crucial role during the interaction between plants and pathogens. Therefore, modeling the plant-pathogen relationship and using the molecules involved in this interaction can help in controlling plant diseases, as pathogens have genes related to resistance against pathogenicity. Thus, it is reasonable to identify and use biological induction agents at a large scale by extracting these compounds.202337742892
8665100.9909A Glyphosate-Based Herbicide Cross-Selects for Antibiotic Resistance Genes in Bacterioplankton Communities. Agrochemicals often contaminate freshwater bodies, affecting microbial communities that underlie aquatic food webs. For example, the herbicide glyphosate has the potential to indirectly select for antibiotic-resistant bacteria. Such cross-selection could occur if the same genes (encoding efflux pumps, for example) confer resistance to both glyphosate and antibiotics. To test for cross-resistance in natural aquatic bacterial communities, we added a glyphosate-based herbicide (GBH) to 1,000-liter mesocosms filled with water from a pristine lake. Over 57 days, we tracked changes in bacterial communities with shotgun metagenomic sequencing and annotated metagenome-assembled genomes (MAGs) for the presence of known antibiotic resistance genes (ARGs), plasmids, and resistance mutations in the enzyme targeted by glyphosate (enolpyruvyl-shikimate-3-phosphate synthase; EPSPS). We found that high doses of GBH significantly increased ARG frequency and selected for multidrug efflux pumps in particular. The relative abundance of MAGs after a high dose of GBH was predictable based on the number of ARGs in their genomes (17% of variation explained) and, to a lesser extent, by resistance mutations in EPSPS. Together, these results indicate that GBHs can cross-select for antibiotic resistance in natural freshwater bacteria. IMPORTANCE Glyphosate-based herbicides (GBHs) such as Roundup formulations may have the unintended consequence of selecting for antibiotic resistance genes (ARGs), as demonstrated in previous experiments. However, the effects of GBHs on ARGs remain unknown in natural aquatic communities, which are often contaminated with pesticides from agricultural runoff. Moreover, the resistance provided by ARGs compared to canonical mutations in the glyphosate target enzyme, EPSPS, remains unclear. Here, we performed a freshwater mesocosm experiment showing that a GBH strongly selects for ARGs, particularly multidrug efflux pumps. These selective effects were evident after just a few days, and the ability of bacteria to survive and thrive after GBH stress was predictable by the number of ARGs in their genomes and, to a lesser extent, by mutations in EPSPS. Intensive GBH application may therefore have the unintended consequence of selecting for ARGs in natural freshwater communities.202235266795
6734110.9909Organic acids enhance bioavailability of tetracycline in water to Escherichia coli for uptake and expression of antibiotic resistance. Tetracyclines are a large class of antimicrobials used most extensively in livestock feeding operations. A large portion of tetracyclines administered to livestock is excreted in manure and urine which is collected in waste lagoons. Subsequent land application of these wastes introduces tetracyclines into the soil environment, where they could exert selective pressure for the development of antibiotic resistance genes in bacteria. Tetracyclines form metal-complexes in natural waters, which could reduce their bioavailability for bacterial uptake. We hypothesized that many naturally-occurring organic acids could effectively compete with tetracyclines as ligands for metal cations, hence altering the bioavailability of tetracyclines to bacteria in a manner that could enhance the selective pressure. In this study, we investigated the influence of acetic acid, succinic acid, malonic acid, oxalic acid and citric acid on tetracycline uptake from water by Escherichia coli bioreporter construct containing a tetracycline resistance gene which induces the emission of green fluorescence when activated. The presence of the added organic acid ligands altered tetracycline speciation in a manner that enhanced tetracycline uptake by E. coli. Increased bacterial uptake of tetracycline and concomitant enhanced antibiotic resistance response were quantified, and shown to be positively related to the degree of organic acid ligand complexation of metal cations in the order of citric acid > oxalic acid > malonic acid > succinic acid > acetic acid. The magnitude of the bioresponse increased with increasing aqueous organic acid concentration. Apparent positive relation between intracellular tetracycline concentration and zwitterionic tetracycline species in aqueous solution indicates that (net) neutral tetracycline is the species which most readily enters E. coli cells. Understanding how naturally-occurring organic acid ligands affect tetracycline speciation in solution, and how speciation influences tetracycline uptake by bacteria, allows more accurate assessment of the selective pressure from trace levels of antibiotics in the environment on microbial communities for preserving and developing antibiotic resistance.201425100186
8292120.9909Exopolysaccharide anchoring creates an extreme resistance to sedimentation. By evolving strains of E. coli that hyper-resist sedimentation, we discovered an uncharacterized mechanism that bacteria can use to remain in suspension indefinitely without expending energy. This unusual phenotype was traced to the anchoring of long colanic acid polymers (CAP) that project from the cell surface. Although each characterized mutant activated this same mechanism, the genes responsible and the strengths of the phenotypes varied. Mutations in rcsC, lpp, igaA, or the yjbEFGH operon were sufficient to stimulate sedimentation resistance, while mutations altering the cps promoter, cdgI, or yjbF provided phenotypic enhancements. The sedimentation resistances changed in response to temperature, growth phase, and carbon source and each mutant exhibited significantly reduced biofilm formation. We discovered that the degree of colony mucoidy exhibited by these mutants was not related to the degree of Rcs pathways activation or to the amount of CAP that was produced; rather, it was related to the fraction of CAP that was shed as a true exopolysaccharide. Therefore, these and other mutations that activate this phenotype are likely to be absent from genetic screens that relied on centrifugation to harvest bacteria. We also found that this anchored CAP form is not linked to LPS cores and may not be attached to the outer membrane.IMPORTANCEBacteria can partition in aqueous environments between surface-dwelling, planktonic, sedimentary, and biofilm forms. Residence in each location provides an advantage depending on nutritional and environmental stresses and a community of a single species is often observed to be distributed throughout two or more of these niches. Another adaptive strategy is to produce an extracellular capsule, which provides an environmental shield for the microbe and can allow escape from predators and immune systems. We discovered that bacteria can either shed or stably anchor capsules to dramatically alter their propensity to sediment. The degree to which the bacteria anchor their capsule is controlled by a stress sensing system, suggesting that anchoring may be used as an adaptive response to severe environmental challenges.202133753470
8613130.9909Insights into the role of extracellular polymeric substances (EPS) in the spread of antibiotic resistance genes. Antibiotic resistance genes (ARG) are prevalent in aquatic environments. Discharge from wastewater treatment plants is an important point source of ARG release into the environment. It has been reported that biological treatment processes may enhance rather than remove ARG because of their presence in sludge. Attenuation of ARG in biotechnological processes has been studied in depth, showing that many microorganisms can secrete complex extracellular polymeric substances (EPS). These EPS can serve as multifunctional elements of microbial communities, involving aspects, such as protection, structure, recognition, adhesion, and physiology. These aspects can influence the interaction between microbial cells and extracellular ARG, as well as the uptake of extracellular ARG by microbial cells, thus changing the transformative capability of extracellular ARG. However, it remains unclear whether EPS can affect horizontal ARG transfer, which is one of the main processes of ARG dissemination. In light of this knowledge gap, this review provides insight into the role of EPS in the transmission of ARGs; furthermore, the mechanism of ARG spread is analyzed, and the molecular compositions and functional properties of EPS are summarized; also, how EPS influence ARG mitigation is addressed, and factors impacting how EPS facilitate ARG during wastewater treatment are summarized. This review provides comprehensive insights into the role of EPS in controlling the transport and fate of ARG during biodegradation processes at the mechanistic level.202438169168
732140.9909Extracellular ATP is an environmental cue in bacteria. In animals and plants, extracellular ATP (eATP) functions as a signal and regulates the immune response. During inflammation, intestinal bacteria are exposed to elevated eATP originating from the mucosa. However, whether bacteria respond to eATP is unclear. Here, we show that non-pathogenic Escherichia coli responds to eATP by modifying its transcriptional and metabolic landscapes. A genome-scale promoter library showed that the response is dependent on time, concentration, and medium and ATP specific. Second messengers and genes related to metabolism, biofilm formation, and envelope stress were regulated downstream of eATP. Metabolomics confirmed that eATP triggers enrichment of compounds with bioactive properties in the host or bacteria. Combined genome-scale modeling revealed modifications to global metabolic and biomass building blocks. Consequently, eATP altered the sensitivity to antibiotics and antimicrobial peptides. Finally, in pathogens, eATP controlled virulence factor expression. Our results indicate that eATP is an environmental cue in prokaryotes, which broadly regulates physiology, antimicrobial resistance, and virulence.202541071676
24150.9909Environmental History Modulates Arabidopsis Pattern-Triggered Immunity in a HISTONE ACETYLTRANSFERASE1-Dependent Manner. In nature, plants are exposed to a fluctuating environment, and individuals exposed to contrasting environmental factors develop different environmental histories. Whether different environmental histories alter plant responses to a current stress remains elusive. Here, we show that environmental history modulates the plant response to microbial pathogens. Arabidopsis thaliana plants exposed to repetitive heat, cold, or salt stress were more resistant to virulent bacteria than Arabidopsis grown in a more stable environment. By contrast, long-term exposure to heat, cold, or exposure to high concentrations of NaCl did not provide enhanced protection against bacteria. Enhanced resistance occurred with priming of Arabidopsis pattern-triggered immunity (PTI)-responsive genes and the potentiation of PTI-mediated callose deposition. In repetitively stress-challenged Arabidopsis, PTI-responsive genes showed enrichment for epigenetic marks associated with transcriptional activation. Upon bacterial infection, enrichment of RNA polymerase II at primed PTI marker genes was observed in environmentally challenged Arabidopsis. Finally, repetitively stress-challenged histone acetyltransferase1-1 (hac1-1) mutants failed to demonstrate enhanced resistance to bacteria, priming of PTI, and increased open chromatin states. These findings reveal that environmental history shapes the plant response to bacteria through the development of a HAC1-dependent epigenetic mark characteristic of a primed PTI response, demonstrating a mechanistic link between the primed state in plants and epigenetics.201424963055
8152160.9909Glutathione S-Transferase Enzymes in Plant-Pathogen Interactions. Plant glutathione S-transferases (GSTs) are ubiquitous and multifunctional enzymes encoded by large gene families. A characteristic feature of GST genes is their high inducibility by a wide range of stress conditions including biotic stress. Early studies on the role of GSTs in plant biotic stress showed that certain GST genes are specifically up-regulated by microbial infections. Later numerous transcriptome-wide investigations proved that distinct groups of GSTs are markedly induced in the early phase of bacterial, fungal and viral infections. Proteomic investigations also confirmed the accumulation of multiple GST proteins in infected plants. Furthermore, functional studies revealed that overexpression or silencing of specific GSTs can markedly modify disease symptoms and also pathogen multiplication rates. However, very limited information is available about the exact metabolic functions of disease-induced GST isoenzymes and about their endogenous substrates. The already recognized roles of GSTs are the detoxification of toxic substances by their conjugation with glutathione, the attenuation of oxidative stress and the participation in hormone transport. Some GSTs display glutathione peroxidase activity and these GSTs can detoxify toxic lipid hydroperoxides that accumulate during infections. GSTs can also possess ligandin functions and participate in the intracellular transport of auxins. Notably, the expression of multiple GSTs is massively activated by salicylic acid and some GST enzymes were demonstrated to be receptor proteins of salicylic acid. Furthermore, induction of GST genes or elevated GST activities have often been observed in plants treated with beneficial microbes (bacteria and fungi) that induce a systemic resistance response (ISR) to subsequent pathogen infections. Further research is needed to reveal the exact metabolic functions of GST isoenzymes in infected plants and to understand their contribution to disease resistance.201830622544
8322170.9908Pathogen-induced damage in Drosophila: Uncoupling disease tolerance from resistance. Immune response against infections can be divided into mechanisms of resistance that ensure active pathogen elimination, and mechanisms of disease tolerance, which include processes that return the host to physiological homeostasis without direct control of pathogen load. Studies on host immune response to infection have targeted mechanisms of resistance, and consequently, these are now well-described in both vertebrates and invertebrates. By comparison, the mechanistic basis of disease tolerance is poorly understood. This is in part because both processes interact and can be difficult to disentangle under an infection scenario. Using the insect model Drosophila melanogaster exposed to its natural entomopathogen, Pseudomonas entomophila, we aimed to tease apart mechanisms of disease tolerance from those of resistance. To this end, we reasoned that the response to oral exposure to heat-killed entomopathogenic bacteria, whilst initially triggering both resistance and disease tolerance mechanisms, would be resolved mainly by disease tolerance alone. Using this method, we observe that oral exposure to heat-killed P. entomophila causes mortality and reduced fecundity in D. melanogaster. We confirm that this reduction in fitness-related traits depends on the duration of the exposure, is sexually dimorphic, and is dependent on the virulence of the bacterium. We also found the microbiota to play a role, with its presence exacerbating the deleterious effect on host survival. In addition, we show that the Imd pathway, but not effector genes, is involved in the process of surviving exposure to HK bacteria. This experimental framework, which may be extended to other systems, can be instrumental towards an understanding of the molecular, genetic, and physiological basis of disease tolerance and its interactions with resistance mechanisms.202540971962
8960180.9908Pyraclostrobin 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
8485190.9908Nonsteroidal anti-inflammatory drug diclofenac accelerates the emergence of antibiotic resistance via mutagenesis. Overuse of antimicrobial agents are generally considered to be a key factor in the occurrence of antibiotic resistance bacteria (ARB). Nevertheless, it is unclear whether ARB can be induced by non-antibiotic chemicals such as nonsteroidal anti-inflammatory drug (NSAID). Thus, the objective of this study is to investigate whether NSAID diclofenac (DCF) promote the emergence of antibiotic resistance in Escherichia coli K12 MG1655. Our results suggested that DCF induced the occurrence of ARB which showed hereditary stability of resistance. Meanwhile, gene variation was identified on chromosome of the ARB, and DCF can cause bacterial oxidative stress and SOS response. Subsequently, transcriptional levels of antioxidant (soxS, sodA, sodC, gor, katG, ahpF) and SOS (recA, lexA, uvrA, uvrB, ruvA, ruvB, dinB, umuC, polB) system-related genes were enhanced. However, the expression of related genes cannot be increased in high-dosage treatment compared with low-dosage samples because of cytotoxicity and cellular damage. Simultaneously, high-dosage DCF decreased the mutation frequency but enhanced the resistance of mutants. Our findings expand our knowledge of the promoting effect on the emergence of ARB caused by DCF. More attention and regulations should be given to these potential ecological and health risks for widespread DCF.202336958653