Decoding the Nano-Silver Resistance Mechanism Switch: Targeted Strategies for Control
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PROVIDER: PRJNA1150138 | ENA |
REPOSITORIES: ENA
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Project description:The increasing prevalence of silver nanoparticle (AgNP) resistances in bacteria,such as Escherichia coli(E. coli) has prompted investigations into resistance mechanisms, sparking a debate between flagellin-mediated AgNP precipitation and copper efflux pump (CusCFBA) activation. Our study unveils a sequential progression of AgNP resistance mechanisms, highlighting the regulatory role of envelope stress, including the CpxRA two-component signal transduction system (cpxRA), the phage shock protein systems (Psp), extracytoplasmic function sigma E factor (σE). Specifically, cyclic AgNP exposure amplifies membrane potential (ΔΨ) by 40%, initiating Phase I resistance characterized by flagellin-mediated AgNP precipitation. Prolonged exposure induces a decline in intracellular pH (ΔpH) and ΔΨ, triggering Phase II Ag tolerance via CusCFBA activation. The regulatory role of cell envelope stress in AgNP resistance transition was validated using knockout mutants, revealing a deficient Phase I/II transition in ΔcpxRA (disrupting the CpxRA signal transduction) or ΔpspABC (inactivation of Psp system) and complete abolition of resistance evolution in ΔrseA (deletion of anti-σ factor rseA gene and continuous expression of σE-dependent stress response).
2024-12-31 | GSE275262 | GEO
Project description:Silver nanoparticles cause toxicity in exposed organisms and are an environmental health concern. The mechanisms of silver nanoparticle toxicity, however, remain unclear. We examined the effects of exposure to silver in nano-, bulk- and ionic forms on zebrafish embryos (Danio rerio) using a Next Generation Sequencing approach in an Illumina platform (High-Throughput SuperSAGE). Significant alterations in gene expression were found for all treatments and many of the gene pathways affected, most notably those associated with oxidative phosphorylation and protein synthesis, overlapped strongly between the three treatments indicating similar mechanisms of toxicity for the three forms of silver studied. Changes in oxidative phosphorylation indicated a down-regulation of this pathway at 24h of exposure, but with a recovery at 48h. This finding was consistent with a dose-dependent decrease in oxygen consumption at 24h, but not at 48h, following exposure to silver ions. Overall, our data provide support for the hypothesis that the toxicity caused by silver nanoparticles is principally associated with bioavailable silver ions in exposed zebrafish embryos. These findings are important in the evaluation of the risk that silver particles may pose to exposed vertebrate organisms. mRNA profiles of whole zebrafish embryos at 24 and 48 hours post-fertilisation (hpf) exposed to silver in nano, bulk and ionic forms were generated by deep sequencing using HT-SuperSAGE (Illumina GA2).
2013-06-17 | E-GEOD-38125 | biostudies-arrayexpress
Project description:The toxicity of silver and zinc oxide nanoparticles is hypothesised to be mediated by dissolved metal ions and cerium dioxide nanoparticles (CeO2 NPs) are hypothesised to induce toxicity specifically by oxidative stress dependant on their surface redox state. To test these hypotheses, RNAseq was applied to characterise the molecular responses of cells to metal nanoparticle and metal ion exposures. The human epithelial lung carcinoma cell line A549 was exposed to different CeO2 NPs with different surface charges, micron-sized and nano-sized silver particles and silver ions, micron-sized and nano-sized zinc oxide particles and zinc ions, or control conditions, for 1 hour, 6 hours and 24 hours. Concentrations were the lower of either EC20 or 128 micrograms/mL. Transcriptional responses were characterised by RNAseq transcriptomics using an Illumina HiSeq2500 .
2018-02-01 | E-MTAB-5734 | biostudies-arrayexpress
Project description:Using medaka fish embryo model, toxic effects of silver nanocolloids (SNC, 3.8M-BM-11.0nm diameter) on developmental morphology and gene expression profile were investigated. SNC caused morphological changes in embryos including cardiovascular malformations, ischemia, underdeveloped central nervous system and eyes, and kyphosis at exposures of 0.5mg/L and 1.0mg/L.. To determine in vivo distribution of SNC, medaka embryos were exposed to 0.5mg/L for 6 days and subjected to ICP-OES analyses. Silver was detected in medaka embryos and chorion at levels of 16.6M-BM-19.3pg and 720M-BM-129pg, respectively. TEM analyses showed SNC adhered to the chorion surface and inside the chorion. On investigation of oxidative mechanism, NAC (0.05mM) rescued all embryos by 96-hr post treatment, while 0.5mM GSH did not. NAC blocked lipid peroxidation. Furthermore, medaka oligo DNA microarray and qRT-PCR were used for gene expression profiling in embryos exposed for 48-hr to 0.05mg/L SNC. Six genes relative to embryogenesis and morphogenesis such as ctsL, Tpm1, RBP, mt, atp2a1 and hox6b6 turned out to be affected and their involvement to the above malformations was implied. In conclusion, SNC causes gross malformations in the cardiovascular and central nervous systems in developing medaka embryos through potentially SNC-affected differential expression of a series of genes related to oxidative stress, embryonic cellular proliferation, and morphological development. Three of the stage-21 medaka embryos per sample were exposed in triplicate to 0mg/L (control) and 0.05mg/L SNC for 48 hours. Therefore, for each exposure condition nine of the stage-21 embryos were prepared and used in the SNC exposure test.
2012-06-16 | E-GEOD-33488 | biostudies-arrayexpress
Project description:Using medaka fish embryo model, toxic effects of silver nanocolloids (SNC, 3.8±1.0nm diameter) on developmental morphology and gene expression profile were investigated. SNC caused morphological changes in embryos including cardiovascular malformations, ischemia, underdeveloped central nervous system and eyes, and kyphosis at exposures of 0.5mg/L and 1.0mg/L.. To determine in vivo distribution of SNC, medaka embryos were exposed to 0.5mg/L for 6 days and subjected to ICP-OES analyses. Silver was detected in medaka embryos and chorion at levels of 16.6±9.3pg and 720±29pg, respectively. TEM analyses showed SNC adhered to the chorion surface and inside the chorion. On investigation of oxidative mechanism, NAC (0.05mM) rescued all embryos by 96-hr post treatment, while 0.5mM GSH did not. NAC blocked lipid peroxidation. Furthermore, medaka oligo DNA microarray and qRT-PCR were used for gene expression profiling in embryos exposed for 48-hr to 0.05mg/L SNC. Six genes relative to embryogenesis and morphogenesis such as ctsL, Tpm1, RBP, mt, atp2a1 and hox6b6 turned out to be affected and their involvement to the above malformations was implied. In conclusion, SNC causes gross malformations in the cardiovascular and central nervous systems in developing medaka embryos through potentially SNC-affected differential expression of a series of genes related to oxidative stress, embryonic cellular proliferation, and morphological development.
2012-06-17 | GSE33488 | GEO
Project description:Silver nanoparticles cause toxicity in exposed organisms and are an environmental health concern. The mechanisms of silver nanoparticle toxicity, however, remain unclear. We examined the effects of exposure to silver in nano-, bulk- and ionic forms on zebrafish embryos (Danio rerio) using a Next Generation Sequencing approach in an Illumina platform (High-Throughput SuperSAGE). Significant alterations in gene expression were found for all treatments and many of the gene pathways affected, most notably those associated with oxidative phosphorylation and protein synthesis, overlapped strongly between the three treatments indicating similar mechanisms of toxicity for the three forms of silver studied. Changes in oxidative phosphorylation indicated a down-regulation of this pathway at 24h of exposure, but with a recovery at 48h. This finding was consistent with a dose-dependent decrease in oxygen consumption at 24h, but not at 48h, following exposure to silver ions. Overall, our data provide support for the hypothesis that the toxicity caused by silver nanoparticles is principally associated with bioavailable silver ions in exposed zebrafish embryos. These findings are important in the evaluation of the risk that silver particles may pose to exposed vertebrate organisms.
2013-06-17 | GSE38125 | GEO
Project description:Transcriptomic changes induced by silver nanoparticles (AgNPs) during spontaneous differentiation of mouse embryonic stem cells (ESCs) were characterized and compared to those induced by Ag+ under otherwise identical conditions. C57BL/6 mESCs were allowed to differentiate after embryoid body (EB) formation and were exposed to 5.0 µg/ml 20 nm AgNPs or 5.0 µg/ml Ag+ for 24 h.
2017-04-07 | GSE79766 | GEO
Project description:Background: The uncontrolled and widespread use of (nano)silver compounds has led to the increased release of these compounds into the environment, raising concerns about their negative impact on ecosystems. Concomitantly, silver resistance determinants are widely spread among environmental and clinically relevant bacteria although the underlying mechanisms are not yet fully understood. Results: In this study, we show that Cupriavidus metallidurans is able to adapt to toxic silver concentrations and explicate the genetic circuit responsible for this adaptation. None of the known silver resistant determinants present in C. metallidurans are involved in the adapted response. Instead, increased silver resistance is achieved by the concerted action of a two-component system AgrR-AgrS, previously not associated with metal resistance, and two intrinsically disordered proteins PrsQ1 and PrsQ2. Both belong to an unique group of small, uncharacterized, extracellular proteins restricted to the genera Cupriavidus and Ralstonia. This system seems to be much more efficient as it gives C. metallidurans the ability to withstand much higher silver concentrations. The latter could be facilitated by the accumulation of silver ions and the formation of silver nanoparticles. Conclusions: Detailed knowledge and exploitation of this protein family could result in novel routes for metal nanoparticle formation and metal processing relevant for biotechnical and biomedical applications.
2018-12-31 | GSE107669 | GEO
Project description:The present work was devoted to a multi-level characterization of E. coli exposed to Ag+-mediated stress using for the first time an approach of integrative biology, based on the combination of physiological, biochemical and transcriptomic data sets. Bacterial growth and survival after Ag+ exposure were first quantified and related to the accumulation of intracellular silver, as detected by Nano Secondary Ion Mass Spectroscopy (NanoSIMS) at high lateral resolution. The whole transcriptomic response of E. coli cells under ionic silver-mediated stress was then characterized. Clear correlations were established between (i) cell physiology, (ii) variations in the biochemical characteristics of cell fatty acids and proteins, and (iii) regulation of gene expression. This challenging approach allowed determining key genetic markers of the E. coli response to ionic silver. In particular, we identified Ag+-mediated regulations of gene expression in correlation with growth (e.g. genes of transporters, transcriptional regulators, ribosomal proteins), necessary for ionic silver transport and detoxification (e.g. copA, cueO, mgtA, nhaR) and to cope with various stress (dnaK, pspA, metA,R, oxidoreductase genes). Regulation of gene expression after Ag+ exposure was also correlated to macromolecular modifications, such as acyl chain length (e.g. fadL, lpxA, arnA), protein secondary structure (e.g. dnaJ, htpX, degP) and cell morphology (e.g. ycfS, ycbB).
2017-02-09 | GSE67735 | GEO
Project description:Comparison of brain gene expression between silver foxes selected for tame behavior and non-selected silver fox.
2005-12-31 | E-MEXP-451 | biostudies-arrayexpress