# | Rank | Similarity | Title + Abs. | Year | PMID |
|---|---|---|---|---|---|
| 0 | 1 | 2 | 3 | 4 | 5 |
| 8283 | 0 | 0.9915 | Stress responses as determinants of antimicrobial resistance in Gram-negative bacteria. Bacteria encounter a myriad of potentially growth-compromising conditions in nature and in hosts of pathogenic bacteria. These 'stresses' typically elicit protective and/or adaptive responses that serve to enhance bacterial survivability. Because they impact upon many of the same cellular components and processes that are targeted by antimicrobials, adaptive stress responses can influence antimicrobial susceptibility. In targeting and interfering with key cellular processes, antimicrobials themselves are 'stressors' to which protective stress responses have also evolved. Cellular responses to nutrient limitation (nutrient stress), oxidative and nitrosative stress, cell envelope damage (envelope stress), antimicrobial exposure and other growth-compromising stresses, have all been linked to the development of antimicrobial resistance in Gram-negative bacteria - resulting from the stimulation of protective changes to cell physiology, activation of resistance mechanisms, promotion of resistant lifestyles (biofilms), and induction of resistance mutations. | 2012 | 22424589 |
| 6442 | 1 | 0.9915 | A systematic review of antibiotic resistance driven by metal-based nanoparticles: Mechanisms and a call for risk mitigation. Elevations in antibiotic resistance genes (ARGs) are due not only to the antibiotic burden, but also to numerous environmental pressures (e.g., pesticides, metal ions, or psychotropic pharmaceuticals), which have led to an international public health emergency. Metal-based nanoparticles (MNPs) poison bacteria while propelling nanoresistance at ambient or sub-lethal concentrations, acting as a wide spectrum germicidal agent. Awareness of MNPs driven antibiotic resistance has created a surge of investigation into the molecule mechanisms of evolving and spreading environmental antibiotic resistome. Co-occurrence of MNPs resistance and antibiotic resistance emerge in environmental pathogens and benign microbes may entail a crucial outcome for human health. In this review we expound on the systematic mechanism of ARGs proliferation under the stress of MNPs, including reactive oxygen species (ROS) induced mutation, horizontal gene transfer (HGT) relevant genes regulation, nano-property, quorum sensing, and biofilm formation and highlighting on the momentous contribution of nanoparticle released ion. As antibiotic resistance pattern alteration is closely knit with the mediate activation of nanoparticle in water, soil, manure, or sludge habitats, we have proposed a virulence and evolution based antibiotic resistance risk assessment strategy for MNP contaminated areas and discussed practicable approaches that call for risk management in critical environmental compartments. | 2024 | 38220012 |
| 8330 | 2 | 0.9915 | Increased iron utilization and oxidative stress tolerance in a Vibrio cholerae flrA mutant confers resistance to amoeba predation. Persistence of V. cholerae in the aquatic environment contributes to the fatal diarrheal disease cholera, which remains a global health burden. In the environment, bacteria face predation pressure by heterotrophic protists such as the free-living amoeba A. castellanii. This study explores how a mutant of V. cholerae adapts to acquire essential nutrients and survive predation. Here, we observed that up-regulation of iron acquisition genes and genes regulating resistance to oxidative stress enhances pathogen fitness. Our data show that V. cholerae can defend predation to overcome nutrient limitation and oxidative stress, resulting in an enhanced survival inside the protozoan hosts. | 2023 | 37882527 |
| 8329 | 3 | 0.9914 | Protozoan predation enhances stress resistance and antibiotic tolerance in Burkholderia cenocepacia by triggering the SOS response. Bacterivorous protists are thought to serve as training grounds for bacterial pathogens by subjecting them to the same hostile conditions that they will encounter in the human host. Bacteria that survive intracellular digestion exhibit enhanced virulence and stress resistance after successful passage through protozoa but the underlying mechanisms are unknown. Here we show that the opportunistic pathogen Burkholderia cenocepacia survives phagocytosis by ciliates found in domestic and hospital sink drains, and viable bacteria are expelled packaged in respirable membrane vesicles with enhanced resistance to oxidative stress, desiccation, and antibiotics, thereby contributing to pathogen dissemination in the environment. Reactive oxygen species generated within the protozoan phagosome promote the formation of persisters tolerant to ciprofloxacin by activating the bacterial SOS response. In addition, we show that genes encoding antioxidant enzymes are upregulated during passage through ciliates increasing bacterial resistance to oxidative radicals. We prove that suppression of the SOS response impairs bacterial intracellular survival and persister formation within protists. This study highlights the significance of protozoan food vacuoles as niches that foster bacterial adaptation in natural and built environments and suggests that persister switch within phagosomes may be a widespread phenomenon in bacteria surviving intracellular digestion. | 2024 | 38366016 |
| 8616 | 4 | 0.9912 | Mechanisms of inhibition and recovery under multi-antibiotic stress in anammox: A critical review. With the escalating global concern for emerging pollutants, particularly antibiotics, microplastics, and nanomaterials, the potential disruption they pose to critical environmental processes like anaerobic ammonia oxidation (anammox) has become a pressing issue. The anammox process, which plays a crucial role in nitrogen removal from wastewater, is particularly sensitive to external pollutants. This paper endeavors to address this knowledge gap by providing a comprehensive overview of the inhibition mechanisms of multi-antibiotic on anaerobic ammonia-oxidizing bacteria, along with insights into their recovery processes. The paper dives deeply into the various ways antibiotics interact with anammox bacteria, focusing specifically on their interference with the bacteria's extracellular polymers (EPS) - crucial components that maintain the structural integrity and functionality of the cells. Additionally, it explores how anammox bacteria utilize quorum sensing (QS) mechanisms to regulate their community structure and respond to antibiotic stress. Moreover, the paper summarizes effective removal methods for these antibiotics from wastewater systems, which is crucial for mitigating their inhibitory effects on anammox bacteria. Finally, the paper offers valuable insights into how anammox communities can recuperate from multi-antibiotic stress. This includes strategies for reintroducing healthy bacteria, optimizing operational conditions, and using bioaugmentation techniques to enhance the resilience of anammox communities. In summary, this paper not only enriches our understanding of the complex interactions between antibiotics and anammox bacteria but also provides theoretical and practical guidance for the treatment of antibiotic pollution in sewage, ensuring the sustainability and effectiveness of wastewater treatment processes. | 2024 | 39366232 |
| 8658 | 5 | 0.9911 | Microplastic 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. | 2025 | 41056669 |
| 8599 | 6 | 0.9911 | Artificial sweeteners stimulate horizontal transfer of extracellular antibiotic resistance genes through natural transformation. Antimicrobial resistance has emerged as a global threat to human health. Natural transformation is an important pathway for horizontal gene transfer, which facilitates the dissemination of antibiotic resistance genes (ARGs) among bacteria. Although it is suspected that artificial sweeteners could exert antimicrobial effects, little is known whether artificial sweeteners would also affect horizontal transfer of ARGs via transformation. Here we demonstrate that four commonly used artificial sweeteners (saccharin, sucralose, aspartame, and acesulfame potassium) promote transfer of ARGs via natural transformation in Acinetobacter baylyi ADP1, a model organism for studying competence and transformation. Such phenomenon was also found in a Gram-positive human pathogen Bacillus subtilis and mice faecal microbiome. We reveal that exposure to these sweeteners increases cell envelope permeability and results in an upregulation of genes encoding DNA uptake and translocation (Com) machinery. In addition, we find that artificial sweeteners induce an increase in plasmid persistence in transformants. We propose a mathematical model established to predict the long-term effects on transformation dynamics under exposure to these sweeteners. Collectively, our findings offer insights into natural transformation promoted by artificial sweeteners and highlight the need to evaluate these environmental contaminants for their antibiotic-like side effects. | 2022 | 34465899 |
| 8619 | 7 | 0.9911 | Bioavailability of pollutants and chemotaxis. The exposure of bacteria to pollutants induces frequently chemoattraction or chemorepellent reactions. Recent research suggests that the capacity to degrade a toxic compound has co-evolved in some bacteria with the capacity to chemotactically react to it. There is an increasing amount of data which show that chemoattraction to biodegradable pollutants increases their bioavailability which translates into an enhancement of the biodegradation rate. Pollutant chemoreceptors so far identified are encoded on degradation or resistance plasmids. Genetic engineering of bacteria, such as the transfer of chemoreceptor genes, offers thus the possibility to optimize biodegradation processes. | 2013 | 22981870 |
| 8635 | 8 | 0.9911 | Techniques for enhancing the tolerance of industrial microbes to abiotic stresses: A review. The diversity of stress responses and survival strategies evolved by microorganism enables them to survive and reproduce in a multitude of harsh environments, whereas the discovery of the underlying resistance genes or mechanisms laid the foundation for the directional enhancement of microbial tolerance to abiotic stresses encountered in industrial applications. Many biological techniques have been developed for improving the stress resistance of industrial microorganisms, which greatly benefited the bacteria on which industrial production is based. This review introduces the main techniques for enhancing the resistance of microorganisms to abiotic stresses, including evolutionary engineering, metabolic engineering, and process engineering, developed in recent years. In addition, we also discuss problems that are still present in this area and offer directions for future research. | 2020 | 31206805 |
| 8612 | 9 | 0.9910 | Nano- 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. | 2024 | 38905974 |
| 9371 | 10 | 0.9910 | Coevolutionary history of predation constrains the evolvability of antibiotic resistance in prey bacteria. Understanding how the historical contingency of biotic interactions shapes the evolvability of bacterial populations is imperative for the predictability of the eco-evolutionary dynamics of microbial communities. While microbial predators like Myxococcus xanthus influence the frequency of antibiotic-resistant bacteria in nature, the effect of adaptation to the presence of predators on the evolvability of prey bacteria to future stressors is unclear. Hence, to understand the influence of the coevolutionary history of predation on the evolvability of antibiotic resistance, we propagated variants of E. coli, pre-adapted to distinct biotic and abiotic conditions, in gradually increasing concentrations of antibiotics. We show that pre-adaptation to predators limits the evolution of a high degree of antibiotic resistance. Moreover, lower degree of resistance in the evolved strains also incurs reduced fitness costs while preserving their ancestral ability to resist predation. Together, we demonstrate that the history of biotic interactions can strongly influence the evolvability of bacteria. | 2025 | 40461734 |
| 728 | 11 | 0.9910 | Surviving Reactive Chlorine Stress: Responses of Gram-Negative Bacteria to Hypochlorous Acid. Sodium hypochlorite (NaOCl) and its active ingredient, hypochlorous acid (HOCl), are the most commonly used chlorine-based disinfectants. HOCl is a fast-acting and potent antimicrobial agent that interacts with several biomolecules, such as sulfur-containing amino acids, lipids, nucleic acids, and membrane components, causing severe cellular damage. It is also produced by the immune system as a first-line of defense against invading pathogens. In this review, we summarize the adaptive responses of Gram-negative bacteria to HOCl-induced stress and highlight the role of chaperone holdases (Hsp33, RidA, Cnox, and polyP) as an immediate response to HOCl stress. We also describe the three identified transcriptional regulators (HypT, RclR, and NemR) that specifically respond to HOCl. Besides the activation of chaperones and transcriptional regulators, the formation of biofilms has been described as an important adaptive response to several stressors, including HOCl. Although the knowledge on the molecular mechanisms involved in HOCl biofilm stimulation is limited, studies have shown that HOCl induces the formation of biofilms by causing conformational changes in membrane properties, overproducing the extracellular polymeric substance (EPS) matrix, and increasing the intracellular concentration of cyclic-di-GMP. In addition, acquisition and expression of antibiotic resistance genes, secretion of virulence factors and induction of the viable but nonculturable (VBNC) state has also been described as an adaptive response to HOCl. In general, the knowledge of how bacteria respond to HOCl stress has increased over time; however, the molecular mechanisms involved in this stress response is still in its infancy. A better understanding of these mechanisms could help understand host-pathogen interactions and target specific genes and molecules to control bacterial spread and colonization. | 2020 | 32796669 |
| 583 | 12 | 0.9910 | MarR family proteins sense sulfane sulfur in bacteria. Members of the multiple antibiotic resistance regulator (MarR) protein family are ubiquitous in bacteria and play critical roles in regulating cellular metabolism and antibiotic resistance. MarR family proteins function as repressors, and their interactions with modulators induce the expression of controlled genes. The previously characterized modulators are insufficient to explain the activities of certain MarR family proteins. However, recently, several MarR family proteins have been reported to sense sulfane sulfur, including zero-valent sulfur, persulfide (R-SSH), and polysulfide (R-SnH, n ≥ 2). Sulfane sulfur is a common cellular component in bacteria whose levels vary during bacterial growth. The changing levels of sulfane sulfur affect the expression of many MarR-controlled genes. Sulfane sulfur reacts with the cysteine thiols of MarR family proteins, causing the formation of protein thiol persulfide, disulfide bonds, and other modifications. Several MarR family proteins that respond to reactive oxygen species (ROS) also sense sulfane sulfur, as both sulfane sulfur and ROS induce the formation of disulfide bonds. This review focused on MarR family proteins that sense sulfane sulfur. However, the sensing mechanisms reviewed here may also apply to other proteins that detect sulfane sulfur, which is emerging as a modulator of gene regulation. | 2024 | 38948149 |
| 726 | 13 | 0.9910 | Regulation of antimicrobial resistance by extracytoplasmic function (ECF) sigma factors. Extracytoplasmic function (ECF) sigma factors are a subfamily of σ(70) sigma factors that activate genes involved in stress-response functions. In many bacteria, ECF sigma factors regulate resistance to antimicrobial compounds. This review will summarize the ECF sigma factors that regulate antimicrobial resistance in model organisms and clinically relevant pathogens. | 2017 | 28153747 |
| 589 | 14 | 0.9909 | Insulin 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. | 2019 | 31244863 |
| 8631 | 15 | 0.9909 | Bacterial metal(loid) resistance genes (MRGs) and their variation and application in environment: A review. Toxic metal(loid)s are widespread and permanent in the biosphere, and bacteria have evolved a wide variety of metal(loid) resistance genes (MRGs) to resist the stress of excess metal(loid)s. Via active efflux, permeability barriers, extracellular/intracellular sequestration, enzymatic detoxification and reduction in metal(loid)s sensitivity of cellular targets, the key components of bacterial cells are protected from toxic metal(loid)s to maintain their normal physiological functions. Exploiting bacterial metal(loid) resistance mechanisms, MRGs have been applied in many environmental fields. Based on the specific binding ability of MRGs-encoded regulators to metal(loid)s, MRGs-dependent biosensors for monitoring environmental metal(loid)s are developed. MRGs-related biotechnologies have been applied to environmental remediation of metal(loid)s by using the metal(loid) tolerance, biotransformation, and biopassivation abilities of MRGs-carrying microorganisms. In this work, we review the historical evolution, resistance mechanisms, environmental variation, and environmental applications of bacterial MRGs. The potential hazards, unresolved problems, and future research directions are also discussed. | 2023 | 36758696 |
| 8614 | 16 | 0.9909 | Polystyrene nanoparticles induce biofilm formation in Pseudomonas aeruginosa. In recent years, micro/nanoplastics have garnered widespread attention due to their ecological risks. In this study, we investigated the effects of polystyrene nanoparticles (PS-NPs) of different sizes on the growth and biofilm formation of Pseudomonas aeruginosa PAO1. The results demonstrated that exposure to certain concentrations of PS-NPs significantly promoted bacterial biofilm formation. Meanwhile, we comprehensively revealed its mechanism whereby PS-NPs induced oxidative stress and altered bacterial membrane permeability by contacting or penetrating bacterial membranes. To counteract the stimulation by PS-NPs and reduce their toxicity, bacteria enhanced biofilm formation by upregulating the expression of biofilm-related genes, increasing EPS and virulence factors secretion, and enhancing bacterial motility through the participation of the quorum sensing (QS) system. Additionally, we also found that exposure to PS-NPs enhanced bacterial antibiotic resistance, posing a challenge to antimicrobial therapy. Our study reveals the toxic effects of nanoplastics and the defense mechanisms of bacteria, which has important implications for the risk assessment and management of environmental nanoplastics. | 2024 | 38442601 |
| 8190 | 17 | 0.9909 | Identification of Quorum-Sensing Inhibitors Disrupting Signaling between Rgg and Short Hydrophobic Peptides in Streptococci. Bacteria coordinate a variety of social behaviors, important for both environmental and pathogenic bacteria, through a process of intercellular chemical signaling known as quorum sensing (QS). As microbial resistance to antibiotics grows more common, a critical need has emerged to develop novel anti-infective therapies, such as an ability to attenuate bacterial pathogens by means of QS interference. Rgg quorum-sensing pathways, widespread in the phylum Firmicutes, employ cytoplasmic pheromone receptors (Rgg transcription factors) that directly bind and elicit gene expression responses to imported peptide signals. In the human-restricted pathogen Streptococcus pyogenes, the Rgg2/Rgg3 regulatory circuit controls biofilm development in response to the short hydrophobic peptides SHP2 and SHP3. Using Rgg-SHP as a model receptor-ligand target, we sought to identify chemical compounds that could specifically inhibit Rgg quorum-sensing circuits. Individual compounds from a diverse library of known drugs and drug-like molecules were screened for their ability to disrupt complexes of Rgg and FITC (fluorescein isothiocyanate)-conjugated SHP using a fluorescence polarization (FP) assay. The best hits were found to bind Rgg3 in vitro with submicromolar affinities, to specifically abolish transcription of Rgg2/3-controlled genes, and to prevent biofilm development in S. pyogenes without affecting bacterial growth. Furthermore, the top hit, cyclosporine A, as well as its nonimmunosuppressive analog, valspodar, inhibited Rgg-SHP pathways in multiple species of Streptococcus. The Rgg-FITC-peptide-based screen provides a platform to identify inhibitors specific for each Rgg type. Discovery of Rgg inhibitors constitutes a step toward the goal of manipulating bacterial behavior for purposes of improving health. IMPORTANCE: The global emergence of antibiotic-resistant bacterial infections necessitates discovery not only of new antimicrobials but also of novel drug targets. Since antibiotics restrict microbial growth, strong selective pressures to develop resistance emerge quickly in bacteria. A new strategy to fight microbial infections has been proposed, namely, development of therapies that decrease pathogenicity of invading organisms while not directly inhibiting their growth, thus decreasing selective pressure to establish resistance. One possible means to this goal is to interfere with chemical communication networks used by bacteria to coordinate group behaviors, which can include the synchronized expression of genes that lead to disease. In this study, we identified chemical compounds that disrupt communication pathways regulated by Rgg proteins in species of Streptococcus. Treatment of cultures of S. pyogenes with the inhibitors diminished the development of biofilms, demonstrating an ability to control bacterial behavior with chemicals that do not inhibit growth. | 2015 | 25968646 |
| 732 | 18 | 0.9909 | Extracellular 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. | 2025 | 41071676 |
| 8633 | 19 | 0.9909 | Bacterial interactions with arsenic: Metabolic pathways, resistance mechanisms, and bioremediation approaches. Arsenic contamination in natural waters is one of the biggest threats to human health, mainly due to its carcinogenic potential. Given its toxicity, nearly all organisms have evolved to develop an arsenic resistance mechanism. Conventional techniques of arsenic remediation suffer from various limitations of their applicability, cost and/or chemical intensive nature. In past few decades, bioremediation has emerged as a potential alternative to the conventional techniques. Microbial bioremediation, bacteria in particular, offers an eco-friendly and sustainable alternative, owing to its inherent metabolic capabilities to transform, immobilize or volatilize arsenic. Diverse biochemical pathways involving oxidation of As(III) to As(V), reduction of As(V) under anaerobic respiration or detoxification, methylation and demethylation, bioleaching and biomineralization into insoluble forms are essential mechanisms for arsenic remediation. These transformations, detoxification and resistance are regulated by specific genetic systems, including the ars operon, aio, arr and arsM, accessory genes such as arsR, arsB, acr3, arsC and arsP. The metabolic regulation of arsenic detoxification involves complex cofactor-dependent enzyme systems and environmental signal-responsive transcriptional control. Integrated approaches such as immobilization of bacteria on biochar or their encapsulation have also been known to enhance stability, reusability and stress tolerance. However, bioremediation is a very complex process due to the interrelationship of various influences such as, presence of specific microorganisms, nutrients and environmental factors. Therefore, it is of utmost importance to understand the bacterial interactions with arsenic for the development of bioremediation technologies. This review article tries to discuss the current status of arsenic bioremediation using bacteria, its field applications, challenges and future perspectives. It also includes the strengths, weaknesses, opportunities, threats (SWOT) analysis to assess the merits and demerits of using bacteria for bioremediation of arsenic. | 2025 | 41043264 |