S_aureus_&_triclosan
Ontology highlight
ABSTRACT:
ORGANISM(S): Staphylococcus aureus
PROVIDER: GSE5799 | GEO | 2008/01/11
SECONDARY ACCESSION(S): PRJNA97167
REPOSITORIES: GEO
Similar Datasets
Project description:A triclosan-ciprofloxacin cross-resistant mutant strain of Staphylococcus aureus displays an alteration in the expression of several cell membrane structural and functional genes. Triclosan is an antimicrobial agent found in many consumer products. Several studies have demonstrated that triclosan inhibits the bacterial fatty acid biosynthetic enzyme, enoyl-ACP reductase (FabI). Studies have also demonstrated that decreased susceptibility to triclosan correlates with ciprofloxacin resistance in several bacteria. In these bacteria, resistance to both drugs maps to genes encoding multi-drug efflux pumps. The focus of this study was to determine whether triclosan resistance contributes to ciprofloxacin resistance in Staphylococcus aureus. Gene expression profiling was performed to compare the gene expression profiles of unexposed and triclosan-exposed wild-type and JJ5 determined that an alteration in global gene expression possibly resulting in a change in cell membrane structure and function is likely responsible for triclosan and ciprofloxacin resistance in JJ5. Keywords: Treatment response WT and triclosan resistant mutant were treated with triclosan and their gene expression was compared to their untreated conterparts.
2010-05-26 | E-GEOD-5799 | biostudies-arrayexpress
Project description:The rise of antibiotic resistance in many bacterial pathogens has been driven by the spread of a few successful strains, suggesting that some bacteria are genetically pre-disposed to evolving resistance. We tested this hypothesis by challenging a diverse set of 222 strains of Staphylococcus aureus with the antibiotic ciprofloxacin in a large-scale evolution experiment. Surprisingly, we found that a single efflux pump, norA, causes widespread variation in evolvability across the diversity of S. aureus. In most lineages of S. aureus, elevated norA expression potentiated evolution by increasing the fitness benefit provided by resistance mutations in DNA topoisomerase under ciprofloxacin treatment. Amplification of norA provided a further mechanism of rapid evolution, but this was restricted to strains from CC398. Crucially, chemically inhibiting NorA effectively prevented the evolution of resistance across the diversity of S. aureus. Our study shows that the underlying genetic diversity of pathogenic bacteria plays a key role in shaping resistance evolution. Understanding this link makes it possible to predict which strains are likely to evolve resistance and to optimize inhibitor use to prevent this outcome.
2020-07-05 | GSE150762 | GEO
Project description:In the present study, we employed Affymetrix Staphylococcus aureus GeneChip arrays to investigate the dynamics of global gene expression profiles during the cellular response of Staphylococcus aureus to triclosan, which involved initial growth inhibition and metabolism. Keywords: Transcriptome study; antimicrobial response; time course
2007-08-25 | GSE8861 | GEO
Project description:Staphylococcus aureus is a leading cause of human disease and can be difficult to treat due to both multi-drug resistance and the organism’s remarkable ability to persist in the host, which is thought to result from several complex regulatory networks that modify transcription in response to environmental stress. In this study, we characterize the global transcriptional response of S. aureus strain 8325 to the antibiotic ciprofloxacin. We find that ciprofloxacin induces prophage mobilization and also significant alterations in metabolism, most notably an upregulation of the tricarboxylic acid cycle. In addition, ciprofloxacin induces the SOS response, which based on a comparison of the wild-type and lexA mutant strains, we show includes the de-repression of sixteen genes. In addition to RecA, LexA, and the hypothetical proteins encoded by SACOL0436, SACOL1375, SACOL1986 and SACOL1999, the S. aureus SOS genes encode proteins involved in DNA metabolism and induced mutation. Finally, we show that rendering LexA uncleavable significantly sensitizes the pathogen to ciprofloxacin therapy in vivo. These observations suggest that the SOS response may play a critical role in the pathogenicity of S. aureus. Keywords: time course
2006-11-30 | GSE6258 | GEO
Project description:Methicillin resistant Staphylococcus aureus (MRSA) infection is becoming refractory to existing antibiotic therapy owing to the inherent ability of S. aureus to develop rapid resistance and is considered a major threat to public health. We found that a natural isolate of Bacillus pumilus from the Columbia River Estuary produces a strong anti-MRSA compound, amicoumacin A. As amicoumacin A has been reported to exhibit anti-microbial, anti-inflammatory, and anti-ulcer activities, we sought to uncover its mechanism of action. Genome-wide transcriptome analysis of S. aureus COL in response to amicoumacin A showed alteration in the expression of genes involved in several cellular processes including cell envelope turnover, cross-membrane transport, virulence, metabolism, and general stress response. The most highly induced gene was lrgA, encoding an antiholin-like product, which has been shown to be induced in response to a collapse of membrane potential. In order to gain further insight into the mechanism of action of amicoumacin A, a whole genome comparison of wild-type COL and amicoumacin A-resistant mutants isolated by serial passage method was carried out. Single point mutations resulting in codon substitutions were uncovered in several distinct genes: ksgA, RNA dimethyltranferase; fusA, elongation factor G; dnaG, primase, ; lacD, tagatose 1,6-bisphosphate aldolase, ; and SACOL0611, encoding a putative glycosyl transferase gene. Based on these results, a candidate approach was undertaken to recreate the same amino acid substitution individually in FusA and KsgA, each of which resulted in two-fold resistance towards amicoumacin A. The fusA gene is known as the site for fusidic acid- resistant mutations; however the codon substitutions in EF-G that cause amicoumacin A resistance and fusidic acid resistance occur in separate domains and do not bring about cross resistance. Taken together, these results suggest that amicoumacin A might cause perturbation of the cell membrane and lead to energy dissipation. Decreased rates of cellular metabolism including protein synthesis and DNA replication in resistant strains might allow cells to compensate for membrane dysfunction and thus increase cell survivability. Amicoumacin A, isolated from Bacillus pumilus, was added to exponentially growing cultures (OD600 =0.5) of Staphylococcus aureus COL at concentrations leading to around 12% and 20% reduction of OD600 after 10 min and 40 min, respectively. Total RNA was isolated from three biological replicates. Labeled cDNA from treated and control cultures (Cy5) was hybridized against a common reference cDNA pool (Cy3). The reference pool was prepared from a mixture of equal amounts of total RNA isolated from all stress and control samples in the experiment.
2012-07-30 | E-GEOD-31342 | biostudies-arrayexpress
Project description:Young adult fer-15;fem-1 Caenorhabditis elegans were infected with Staphylococcus aureus for 8 h to determine the transcriptional host response to Staphylococcus aureus. Analysis of differential gene expression in C. elegans young adults exposed to two different bacteria: E. coli strain OP50 (control), wild-type Staphylococcus aureus RN6390. Samples were analyzed at 8 hours after exposure to the different bacteria. These studies identified C. elegans genes induced by pathogen infection. Keywords: response to pathogen infection, innate immunity, host-pathogen interactions
2010-06-12 | GSE21819 | GEO
Project description:Expressed on epidermal Langerhans cells, CD1a presents a range of self-lipid antigens found within the skin. However, the extent to which CD1a presents microbial ligands from skin bacteria is unclear. Here, we identified CD1a-dependent T cell responses to phosphatidylglycerol (PG), a ubiquitous bacterial membrane phospholipid, as well as to lysyl phosphatidylglycerol (lysylPG), a modified PG, present in the many gram positive bacteria, and highly abundant in Staphylococcus aureus. Specifically, PG and lysylPG together constitute the vast majority of the structural membrane lipids in Staphylococcus aureus. The crystal structure of the CD1a-lysylPG complex showed that the acyl chains were buried within the A′- and F′-pockets of CD1a, while the lysine-modified phosphoglycerol headgroup protruded from the F′-portal and was available for T cell receptor contact. Using lysylPG-loaded CD1a tetramers, we identified T cells in peripheral blood and in skin that respond to this lipid in a dose dependent manner. Tetramer+ CD4+ T cell lines secreted Th2 cytokines in response to lysylPG as well as to co-cultures of CD1a+ dendritic cells and Staphylococcus aureus. The expansion of CD4+ CD1a-lysylPG tetramer+ T cells in atopic dermatitis patients, indicates a response to a lipid made by bacteria associated with atopic dermatitis, and provide a link supporting involvement of PG-based lipid-specific T cells in the pathogenesis of dermatitis.
2022-12-19 | GSE186459 | GEO
Project description:To study the effect of Radix Paeoniae Rubra decoction on tolerance of Staphylococcus aureus.The effect of Radix Paeoniae Rubra on the resistance of Staphylococcus aureus to oxacillin sodium was studied by millipore dilution method in this experiment.At the same time ,conducted on transcriptome analysis of Staphylococcus aureus related genes in Radix Paeoniae Rubra.And to detect the expression level of related genes of Staphylococcus aureus under the action of Radix Paeoniae Rubra by PCR technology.The tolerance of Staphylococcus aureus was decreased obviously when the concentration of Radix Paeoniae Rubra decoction was above 1mg/ml.The effect of Radix Paeoniae Rubra decoction on the expression of tolerance genes femB,pvL and gluM when the concentration of Radix Paeoniae Rubra decoction was above 4mg/ml.When rhe concentration of Radix Paeoniae Rubra is more than 1mg/ml,it can effectively reduce the resistance of Staphylococcus aureus to oxacillin sodium.The reason may be due to the effect of Radix Paeoniae Rubra on the resistance gene of Staphylococcus aureus.
2021-01-30 | GSE165791 | GEO
Project description:Becker2005 - Genome-scale metabolic network
of Staphylococcus aureus (iSB619)
This model is described in the article:
Genome-scale reconstruction
of the metabolic network in Staphylococcus aureus N315: an
initial draft to the two-dimensional annotation.
Becker SA, Palsson BØ.
BMC Microbiol. 2005; 5: 8
Abstract:
BACKGROUND: Several strains of bacteria have sequenced and
annotated genomes, which have been used in conjunction with
biochemical and physiological data to reconstruct genome-scale
metabolic networks. Such reconstruction amounts to a
two-dimensional annotation of the genome. These networks have
been analyzed with a constraint-based formalism and a variety
of biologically meaningful results have emerged. Staphylococcus
aureus is a pathogenic bacterium that has evolved resistance to
many antibiotics, representing a significant health care
concern. We present the first manually curated elementally and
charge balanced genome-scale reconstruction and model of S.
aureus' metabolic networks and compute some of its properties.
RESULTS: We reconstructed a genome-scale metabolic network of
S. aureus strain N315. This reconstruction, termed iSB619,
consists of 619 genes that catalyze 640 metabolic reactions.
For 91% of the reactions, open reading frames are explicitly
linked to proteins and to the reaction. All but three of the
metabolic reactions are both charge and elementally balanced.
The reaction list is the most complete to date for this
pathogen. When the capabilities of the reconstructed network
were analyzed in the context of maximal growth, we formed
hypotheses regarding growth requirements, the efficiency of
growth on different carbon sources, and potential drug targets.
These hypotheses can be tested experimentally and the data
gathered can be used to improve subsequent versions of the
reconstruction. CONCLUSION: iSB619 represents comprehensive
biochemically and genetically structured information about the
metabolism of S. aureus to date. The reconstructed metabolic
network can be used to predict cellular phenotypes and thus
advance our understanding of a troublesome pathogen.
This model is hosted on
BioModels Database
and identified by:
MODEL1507180070.
To cite BioModels Database, please use:
BioModels Database:
An enhanced, curated and annotated resource for published
quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2024-10-15 | MODEL1507180070 | BioModels
Project description:Methicillin resistant Staphylococcus aureus (MRSA) infection is becoming refractory to existing antibiotic therapy owing to the inherent ability of S. aureus to develop rapid resistance and is considered a major threat to public health. We found that a natural isolate of Bacillus pumilus from the Columbia River Estuary produces a strong anti-MRSA compound, amicoumacin A. As amicoumacin A has been reported to exhibit anti-microbial, anti-inflammatory, and anti-ulcer activities, we sought to uncover its mechanism of action. Genome-wide transcriptome analysis of S. aureus COL in response to amicoumacin A showed alteration in the expression of genes involved in several cellular processes including cell envelope turnover, cross-membrane transport, virulence, metabolism, and general stress response. The most highly induced gene was lrgA, encoding an antiholin-like product, which has been shown to be induced in response to a collapse of membrane potential. In order to gain further insight into the mechanism of action of amicoumacin A, a whole genome comparison of wild-type COL and amicoumacin A-resistant mutants isolated by serial passage method was carried out. Single point mutations resulting in codon substitutions were uncovered in several distinct genes: ksgA, RNA dimethyltranferase; fusA, elongation factor G; dnaG, primase, ; lacD, tagatose 1,6-bisphosphate aldolase, ; and SACOL0611, encoding a putative glycosyl transferase gene. Based on these results, a candidate approach was undertaken to recreate the same amino acid substitution individually in FusA and KsgA, each of which resulted in two-fold resistance towards amicoumacin A. The fusA gene is known as the site for fusidic acid- resistant mutations; however the codon substitutions in EF-G that cause amicoumacin A resistance and fusidic acid resistance occur in separate domains and do not bring about cross resistance. Taken together, these results suggest that amicoumacin A might cause perturbation of the cell membrane and lead to energy dissipation. Decreased rates of cellular metabolism including protein synthesis and DNA replication in resistant strains might allow cells to compensate for membrane dysfunction and thus increase cell survivability.
2012-07-31 | GSE31342 | GEO