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73400.9893Mechanisms of Keap1/Nrf2 modulation in bacterial infections: implications in persistence and clearance. Pathogenic bacteria trigger complex molecular interactions in hosts that are characterized mainly by an increase in reactive oxygen species (ROS) as well as an inflammation-associated response. To counteract oxidative damage, cells respond through protective mechanisms to promote resistance and avoid tissue damage and infection; among these cellular mechanisms the activation or inhibition of the nuclear factor E2-related factor 2 (Nrf2) is frequently observed. The transcription factor Nrf2 is considered the master regulator of several hundred cytoprotective and antioxidant genes. Under normal conditions, the Keap1/Nrf2 signaling protects the cellular environment by sensing deleterious oxygen radicals and inducing the expression of genes coding for proteins intended to neutralize the harmful effects of ROS. However, bacteria have developed strategies to harness Nrf2 activity to their own benefit, complicating the host response. This review is aimed to present the most recent information and probable mechanisms employed by a variety of bacteria to modulate the Keap1/Nrf2 activity in order to survive in the infected tissue. Particularly, those utilized by the Gram-positive bacteria Staphylococcus aureus, Streptococcus pneumoniae, Listeria monocytogenes, and Mycobacterium tuberculosis as well as by the Gram-negative bacteria Escherichia coli, Helicobacter pylori, Legionella pneumophila, Pseudomonas aeruginosa and Salmonella typhimurium. We also discuss and highlight the beneficial impact of the Keap1/Nrf2 antioxidant and anti-inflammatory role in bacterial clearance.202439763664
693410.9889Impact of protist predation on bacterial community traits in river sediments. Sediment-associated microbial communities are pivotal in driving biogeochemical processes and serve as key indicators of ecosystem health and function. However, the ecological impact of protist predation on these microbial communities remains poorly understood. Here, sediment microcosms were established with varying concentrations of indigenous protists. Results revealed that protist predation exerted strong and differential effects on the bacterial community composition, functional capabilities, and antibiotic resistance profiles. Higher levels of protist predation pressure increased bacterial alpha diversity and relative abundance of genera associated with carbon and nitrogen cycling, such as Fusibacter, Methyloversatilis, Azospirillum, and Holophaga. KEGG analysis indicated that protist predation stimulated microbial processes related to the carbon, nitrogen, and sulfur cycles. Notably, the relative abundance and associated health risks of antibiotic resistance genes (ARGs), virulence factor genes (VFGs), and mobile genetic elements (MGEs) were affected by predation pressure. Medium protist predation pressure increased the relative abundance and potential risks associated with ARGs, whereas high protist concentrations led to a reduction in both, likely due to a decrease in the relative abundance of ARG-hosting pathogenic bacteria such as Pseudomonas, Acinetobacter, and Aeromonas. These findings provide comprehensive insights into the dynamics of bacterial communities under protist predation in river sediment ecosystems.202540885182
58620.9889Iron metabolism and resistance to infection by invasive bacteria in the social amoeba Dictyostelium discoideum. Dictyostelium cells are forest soil amoebae, which feed on bacteria and proliferate as solitary cells until bacteria are consumed. Starvation triggers a change in life style, forcing cells to gather into aggregates to form multicellular organisms capable of cell differentiation and morphogenesis. As a soil amoeba and a phagocyte that grazes on bacteria as the obligate source of food, Dictyostelium could be a natural host of pathogenic bacteria. Indeed, many pathogens that occasionally infect humans are hosted for most of their time in protozoa or free-living amoebae, where evolution of their virulence traits occurs. Due to these features and its amenability to genetic manipulation, Dictyostelium has become a valuable model organism for studying strategies of both the host to resist infection and the pathogen to escape the defense mechanisms. Similarly to higher eukaryotes, iron homeostasis is crucial for Dictyostelium resistance to invasive bacteria. Iron is essential for Dictyostelium, as both iron deficiency or overload inhibit cell growth. The Dictyostelium genome shares with mammals many genes regulating iron homeostasis. Iron transporters of the Nramp (Slc11A) family are represented with two genes, encoding Nramp1 and Nramp2. Like the mammalian ortholog, Nramp1 is recruited to phagosomes and macropinosomes, whereas Nramp2 is a membrane protein of the contractile vacuole network, which regulates osmolarity. Nramp1 and Nramp2 localization in distinct compartments suggests that both proteins synergistically regulate iron homeostasis. Rather than by absorption via membrane transporters, iron is likely gained by degradation of ingested bacteria and efflux via Nramp1 from phagosomes to the cytosol. Nramp gene disruption increases Dictyostelium sensitivity to infection, enhancing intracellular growth of Legionella or Mycobacteria. Generation of mutants in other "iron genes" will help identify genes essential for iron homeostasis and resistance to pathogens.201324066281
876630.9888Partitioning 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
855940.9888PFOA and a dash of aluminum: The perfect recipe for growing drug-resistant biofilms in urban water supply. This study investigated the impact of perfluorooctanoic acid (PFOA) and aluminum (Al(III)) on the proliferation of drug-resistant pathogenic bacteria in drinking water distribution system (DWDS) biofilms, and their combined effect. Experimental simulations of stagnant residential water conditions, analyzed via comprehensive metagenomics, revealed a significant increase in bacterial biomass, extracellular polymeric substances (EPS), and the abundance of pathogenic bacteria and antibiotic resistance genes (ARGs). Biofilm formation was markedly enhanced in the presence of PFOA and Al(III), creating protective niches that facilitated the proliferation of pathogenic bacteria and ARGs. Key observations included increases in Legionella pneumophila and Pseudomonas aeruginosa, along with a shift in ARG profiles towards antibiotic efflux and target protection mechanisms. Critically, this study identified the presence and dynamics of priority drug-resistant pathogens within these biofilms, providing essential insights into pollutant-influenced risks and transmission pathways. These findings highlight the significant public health implications of PFOA and Al(III) co-contamination in drinking water systems.202540885069
788950.9887The interaction between extracellular polymeric substances and corrosion products in pipes shaped different bacterial communities and the effects of micropollutants. There are growing concerns over the effects of micropollutants on biofilms formation and antibiotic resistance gene (ARGs) transmission in drinking water distribution pipes. However, there was no reports about the influence of the interaction between extracellular polymeric substances (EPS) and corrosion products on biofilms formation. Our results indicated that the abundance of quorum sensing (QS)-related genes, polysaccharide and amino acids biosynthesis genes of EPS was 6747-8055 TPM, 2221-2619 TPM, and 1461-1535 TPM in biofilms of cast iron pipes, respectively, which were higher than that of stainless steel pipes. The two-dimensional correlation spectroscopy (2D-COS) analysis of attenuated total reflectance-Fourier transform infrared spectrometry (ATR-FTIR) results indicated that polysaccharide of EPS was more easily adsorbed onto the corrosion products of cast iron pipes. Therefore, more human pathogenic bacteria (HPB) carrying ARGs were formed in biofilms of cast iron pipes. The amide I and amide II components and phosphate moieties of EPS were more susceptible to the corrosion products of stainless steel pipes. Thus, more bacteria genera carrying mobile genetic elements (MGE)-ARG were formed in biofilms of stainless steel pipes due to more abundance of QS-related genes, amino acids biosynthesis genes of EPS and the functional genes related to lipid metabolism. The enrichment of dimethyl phthalate (DMP), perfluorooctanoic acid (PFOA) and sulfadiazine (SUL) in corrosion products induced upregulation of QS and EPS-related genes, which promoted bacteria carrying different ARGs growth in biofilms, inducing more microbial risks.202337950951
865860.9886Microplastic exposure reshapes the virome and virus-bacteria networks with implications for immune regulation in Mytilus coruscus. Microplastic pollution has emerged as a critical environmental concern, yet its impacts on host-associated viral communities and immune balance in marine bivalves remain largely unexplored. In this study, Mytilus coruscus individuals were exposed to microplastics in situ for seven days. Virome sequencing and bioinformatic analyses revealed that microplastic exposure induced divergent responses in DNA and RNA viral communities. DNA viromes exhibited suppressed diversity and downregulation of core viral metabolic pathways, potentially reflecting reduced viral replication capacity under host immune stress. In contrast, RNA viromes displayed metabolic activation and functional shifts, including enriched glycan and nucleotide metabolism, possibly linked to enhanced viral activity or immune evasion. Phage-bacteria interaction networks were also restructured, showing increased associations with opportunistic pathogens such as Vibrio cholerae and Enterobacter, potentially affecting immune surveillance. Furthermore, the expression of antibiotic resistance genes (ARGs) in viral genomes was differentially regulated, suggesting pollutant-induced microbial selection that may challenge host immune resilience. These findings suggest that microplastics not only reshape virome composition and metabolic functions but also influence virus-mediated immune interactions, with important implications for disease susceptibility and immune homeostasis in filter-feeding shellfish.202541056669
868870.9885Adaptation of intertidal biofilm communities is driven by metal ion and oxidative stresses. Marine organisms in intertidal zones are subjected to periodical fluctuations and wave activities. To understand how microbes in intertidal biofilms adapt to the stresses, the microbial metagenomes of biofilms from intertidal and subtidal zones were compared. The genes responsible for resistance to metal ion and oxidative stresses were enriched in both 6-day and 12-day intertidal biofilms, including genes associated with secondary metabolism, inorganic ion transport and metabolism, signal transduction and extracellular polymeric substance metabolism. In addition, these genes were more enriched in 12-day than 6-day intertidal biofilms. We hypothesize that a complex signaling network is used for stress tolerance and propose a model illustrating the relationships between these functions and environmental metal ion concentrations and oxidative stresses. These findings show that bacteria use diverse mechanisms to adapt to intertidal zones and indicate that the community structures of intertidal biofilms are modulated by metal ion and oxidative stresses.201324212283
58980.9885Insulin 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
856190.9884Three-dimensional synergistic mechanism ofphysical injury, microbiota dysbiosis, and gene transfer in the gut of Cipangopaludina cathayensisunder microplastics and roxithromycin exposure. Microplastics (MPs) and antibiotics pose a combined threat to aquatic organisms by impairing gut health and promoting the spread of antibiotic resistance genes (ARGs). In this study, Cipangopaludina cathayensis was exposed for 28 days to polystyrene MPs, roxithromycin (ROX), and their combination to assess impacts on intestinal barrier integrity, microbiota composition, and ARG proliferation. MPs alone caused significant mucosal damage, villus atrophy, epithelial shedding, and reduced digestive enzyme activities. ROX exposure altered microbiota structure by increasing Bacteroidetes and reducing Firmicutes. Co-exposure (CM group) exacerbated epithelial injury and enzyme inhibition but partially restored balance through enrichment of SCFA-producing, anti-inflammatory bacteria. ARG levels in the CM group rose by over 1000 %, with notable increases in multidrug resistance genes (e.g., blaOXA10) and integrons (e.g., cIntI-1), mainly linked to Bacteroides and Proteobacteria. Transcriptomic data indicated oxidative stress and epithelial disruption under MPs, and upregulation of efflux and integron genes with ROX. Combined exposure triggered DNA repair and SOS pathways, facilitating horizontal gene transfer. These findings highlight a three-dimensional synergistic mechanism-physical damage, microbial dysbiosis, and gene transfer-that amplifies ARG dissemination and intestinal toxicity, underscoring the need to assess ecological risks of composite pollutants in freshwater systems.These processes form a self-reinforcing loop in which physical epithelial damage promotes microbial dysbiosis, which in turn facilitates ARG proliferation through increased permeability and immune disruption.202541067103
587100.9884The Nramp (Slc11) proteins regulate development, resistance to pathogenic bacteria and iron homeostasis in Dictyostelium discoideum. The Dictyostelium discoideum genome harbors two genes encoding members of the Nramp superfamily, which is conserved from bacteria (MntH proteins) to humans (Slc11 proteins). Nramps are proton-driven metal ion transporters with a preference for iron and manganese. Acquisition of these metal cations is vital for all cells, as they act as redox cofactors and regulate key cellular processes, such as DNA synthesis, electron transport, energy metabolism and oxidative stress. Dictyostelium Nramp1 (Slc11a1), like its mammalian ortholog, mediates resistance to infection by invasive bacteria. We have extended the analysis to the nramp2 gene, by generating single and double nramp1/nramp2 knockout mutants and cells expressing GFP fusion proteins. In contrast to Nramp1, which is recruited to phagosomes and macropinosomes, the Nramp2 protein is localized exclusively in the membrane of the contractile vacuole, a vesicular tubular network regulating cellular osmolarity. Both proteins colocalize with the V-H(+)-ATPase, which can provide the electrogenic force for vectorial transport. Like nramp1, nramp2 gene disruption affects resistance to Legionella pneumophila. Disrupting both genes additionally leads to defects in development, with strong delay in cell aggregation, formation of large streams and multi-tipped aggregates. Single and double mutants display differential sensitivity to cell growth under conditions of iron overload or depletion. The data favor the hypothesis that Nramp1 and Nramp2, under control of the V-H(+)-ATPase, synergistically regulate iron homeostasis, with the contractile vacuole possibly acting as a store for metal cations.201322992462
8321110.9884Pathogen Resistance Mediated by IL-22 Signaling at the Epithelial-Microbiota Interface. Intestinal colonization resistance to bacterial pathogens is generally associated, among other factors, with mucosal homeostasis that preserves the integrity of the intestinal barrier. Mucosal homeostasis depends on physical and molecular interactions between three components: the resident microbiota, the epithelial layer and the local immune system. The cytokine IL-22 helps to orchestrate this three-way interaction. IL-22 is produced by immune cells present beneath the epithelium and is induced by bacteria present in the intestine. IL-22 stimulates the epithelial cells via the IL-22RA1-IL-10R2 receptor complex inducing changes in the expression of genes involved in the maintenance of epithelial barrier integrity, with a variety of functions in pathogen resistance such as mucus layer modifications and hydration, tight junction fortification and the production of a broad range of bactericidal compounds. These mechanisms of pathogen resistance, in turn, affect the microbiota composition and create an environment that excludes pathogens. Here we highlight the role of IL-22 as key mediator in the give-and-take relationship between the microbiota and the host that impacts pathogen resistance.201526497621
8646120.9882A Degeneration Gradient of Poplar Trees Contributes to the Taxonomic, Functional, and Resistome Diversity of Bacterial Communities in Rhizosphere Soils. Bacterial communities associated with roots influence the health and nutrition of the host plant. However, the microbiome discrepancy are not well understood under different healthy conditions. Here, we tested the hypothesis that rhizosphere soil microbial diversity and function varies along a degeneration gradient of poplar, with a focus on plant growth promoting bacteria (PGPB) and antibiotic resistance genes. Comprehensive metagenomic analysis including taxonomic investigation, functional detection, and ARG (antibiotics resistance genes) annotation revealed that available potassium (AK) was correlated with microbial diversity and function. We proposed several microbes, Bradyrhizobium, Sphingomonas, Mesorhizobium, Nocardioides, Variovorax, Gemmatimonadetes, Rhizobacter, Pedosphaera, Candidatus Solibacter, Acidobacterium, and Phenylobacterium, as candidates to reflect the soil fertility and the plant health. The highest abundance of multidrug resistance genes and the four mainly microbial resistance mechanisms (antibiotic efflux, antibiotic target protection, antibiotic target alteration, and antibiotic target replacement) in healthy poplar rhizosphere, corroborated the relationship between soil fertility and microbial activity. This result suggested that healthy rhizosphere soil harbored microbes with a higher capacity and had more complex microbial interaction network to promote plant growing and reduce intracellular levels of antibiotics. Our findings suggested a correlation between the plant degeneration gradient and bacterial communities, and provided insight into the role of high-turnover microbial communities as well as potential PGPB as real-time indicators of forestry soil quality, and demonstrated the inner interaction contributed by the bacterial communities.202133810508
8644130.9882Biotic and abiotic drivers of soil carbon, nitrogen and phosphorus and metal dynamic changes during spontaneous restoration of Pb-Zn mining wastelands. The biotic and abiotic mechanisms that drive important biogeochemical processes (carbon, nitrogen, phosphorus and metals dynamics) in metal mine revegetation remains elusive. Metagenomic sequencing was used to explored vegetation, soil properties, microbial communities, functional genes and their impacts on soil processes during vegetation restoration in a typical Pb-Zn mine. The results showed a clear niche differentiation between bacteria, fungi and archaea. Compared to bacteria and fungi, the archaea richness were more tightly coupled with natural restoration changes. The relative abundances of CAZyme-related, denitrification-related and metal resistance genes reduced, while nitrification, urease, inorganic phosphorus solubilisation, phosphorus transport, and phosphorus regulation -related genes increased. Redundancy analysis, hierarchical partitioning analysis, relative-importance analysis and partial least squares path modelling, indicated that archaea diversity, primarily influenced by available lead, directly impacts carbon dynamics. Functional genes, significantly affected by available cadmium, directly alter nitrogen dynamics. Additionally, pH affects phosphorus dynamics through changes in bacterial diversity, while metal dynamics are directly influenced by vegetation. These insights elucidate natural restoration mechanisms in mine and highlight the importance of archaea in soil processes.202540054196
615140.9882Escherichia coli RclA is a highly active hypothiocyanite reductase. Hypothiocyanite and hypothiocyanous acid (OSCN(-)/HOSCN) are pseudohypohalous acids released by the innate immune system which are capable of rapidly oxidizing sulfur-containing amino acids, causing significant protein aggregation and damage to invading bacteria. HOSCN is abundant in saliva and airway secretions and has long been considered a highly specific antimicrobial that is nearly harmless to mammalian cells. However, certain bacteria, commensal and pathogenic, are able to escape damage by HOSCN and other harmful antimicrobials during inflammation, which allows them to continue to grow and, in some cases, cause severe disease. The exact genes or mechanisms by which bacteria respond to HOSCN have not yet been elucidated. We have found, in Escherichia coli, that the flavoprotein RclA, previously implicated in reactive chlorine resistance, reduces HOSCN to thiocyanate with near-perfect catalytic efficiency and strongly protects E. coli against HOSCN toxicity. This is notable in E. coli because this species thrives in the chronically inflamed environment found in patients with inflammatory bowel disease and is able to compete with and outgrow other important commensal organisms, suggesting that HOSCN may be a relevant antimicrobial in the gut, which has not previously been explored. RclA is conserved in a variety of epithelium-colonizing bacteria, implicating its HOSCN reductase activity in a variety of host-microbe interactions. We show that an rclA mutant of the probiotic Limosilactobacillus reuteri is sensitive to HOSCN and that RclA homologs from Staphylococcus aureus, Streptococcus pneumoniae, and Bacteroides thetaiotaomicron all have potent protective activity against HOSCN when expressed in E. coli.202235867824
8612150.9882Nano- and microplastics drive the dynamic equilibrium of amoeba-associated bacteria and antibiotic resistance genes. As emerging pollutants, microplastics have become pervasive on a global scale, inflicting significant harm upon ecosystems. However, the impact of these microplastics on the symbiotic relationship between protists and bacteria remains poorly understood. In this study, we investigated the mechanisms through which nano- and microplastics of varying sizes and concentrations influence the amoeba-bacterial symbiotic system. The findings reveal that nano- and microplastics exert deleterious effects on the adaptability of the amoeba host, with the magnitude of these effects contingent upon particle size and concentration. Furthermore, nano- and microplastics disrupt the initial equilibrium in the symbiotic relationship between amoeba and bacteria, with nano-plastics demonstrating a reduced ability to colonize symbiotic bacteria within the amoeba host when compared to their microplastic counterparts. Moreover, nano- and microplastics enhance the relative abundance of antibiotic resistance genes and heavy metal resistance genes in the bacteria residing within the amoeba host, which undoubtedly increases the potential transmission risk of both human pathogens and resistance genes within the environment. In sum, the results presented herein provide a novel perspective and theoretical foundation for the study of interactions between microplastics and microbial symbiotic systems, along with the establishment of risk assessment systems for ecological environments and human health.202438905974
8292160.9882Exopolysaccharide 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
8613170.9882Insights 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
8648180.9882Host-specific assembly of phycosphere microbiome and enrichment of the associated antibiotic resistance genes: Integrating species of microalgae hosts, developmental stages and water contamination. Phytoplankton-bacteria interactions profoundly impact ecosystem function and biogeochemical cycling, while their substantial potential to carry and disseminate antibiotic resistance genes (ARGs) poses a significant threat to global One Health. However, the ecological paradigm behind the phycosphere assembly of microbiomes and the carrying antibiotic resistomes remains unclear. Our field investigation across various freshwater ecosystems revealed a substantial enrichment of bacteria and ARGs within microalgal niches. Taking account of the influence for species of microalgae hosts, their developmental stages and the stress of water pollution, we characterized the ecological processes governing phycosphere assembly of bacterial consortia and enrichment of the associated ARGs. By inoculating 6 axenic algal hosts with two distinct bacterial consortia from a natural river and the phycosphere of Scenedesmus acuminatus, we observed distinct phycosphere bacteria recruitment among different algal species, yet consistency within the same species. Notably, a convergent bacterial composition was established for the same algae species for two independent inoculations, demonstrating host specificity in phycosphere microbiome assembly. Host-specific signature was discernible as early as the algal lag phase and more pronounced as the algae developed, indicating species types of algae determined mutualism between the bacterial taxa and hosts. The bacteria community dominated the shaping of ARG profiles within the phycosphere and the host-specific phycosphere ARG enrichment was intensified with the algae development. The polluted water significantly stimulated host's directional selection on phycosphere bacterial consortia and increased the proliferation antibiotic resistome. These consortia manifested heightened beneficial functionality, enhancing microalgal adaptability to contamination stress.202540349825
9388190.9881Suboptimal environmental conditions prolong phage epidemics in bacterial populations. Infections by filamentous phages, which are usually nonlethal to the bacterial cells, influence bacterial fitness in various ways. While phage-encoded accessory genes, for example virulence genes, can be highly beneficial, the production of viral particles is energetically costly and often reduces bacterial growth. Consequently, if costs outweigh benefits, bacteria evolve resistance, which can shorten phage epidemics. Abiotic conditions are known to influence the net-fitness effect for infected bacteria. Their impact on the dynamics and trajectories of host resistance evolution, however, remains yet unknown. To address this, we experimentally evolved the bacterium Vibrio alginolyticus in the presence of a filamentous phage at three different salinity levels, that is (1) ambient, (2) 50% reduction and (3) fluctuations between reduced and ambient. In all three salinities, bacteria rapidly acquired resistance through super infection exclusion (SIE), whereby phage-infected cells acquired immunity at the cost of reduced growth. Over time, SIE was gradually replaced by evolutionary fitter surface receptor mutants (SRM). This replacement was significantly faster at ambient and fluctuating conditions compared with the low saline environment. Our experimentally parameterized mathematical model explains that suboptimal environmental conditions, in which bacterial growth is slower, slow down phage resistance evolution ultimately prolonging phage epidemics. Our results may explain the high prevalence of filamentous phages in natural environments where bacteria are frequently exposed to suboptimal conditions and constantly shifting selections regimes. Thus, our future ocean may favour the emergence of phage-born pathogenic bacteria and impose a greater risk for disease outbreaks, impacting not only marine animals but also humans.202437337348