Profiling the effect of Nafcillin on HA-MRSA D712 using bacteriological and physiological media
Ontology highlight
ABSTRACT:
ORGANISM(S): Staphylococcus aureus
PROVIDER: GSE139141 | GEO | 2019/10/22
REPOSITORIES: GEO
Similar Datasets
Project description:The gastric adenocarcinoma cell line HGC-27 and colorectal adenocarcinoma cell line HCT-8 cells were grown in Roswell Park Memorial Institute (RPMI) 1640 medium (Hyclone, Logan, UT, USA.). The human hepatocellular carcinoma cell lines HepG2 and Huh-7 were cultured in Dulbecco’s modified Eagle's medium (DMEM) (Hyclone, Logan, UT, USA.).
2019-06-04 | GSE132119 | GEO
Project description:Background: Telavancin is a novel semi-synthetic lipoglycopeptide derivative of vancomycin with a decylaminoethyl side chain that is active against Gram-positive bacteria including Staphylococcus aureus strains resistant to methicillin or vancomycin. This study describes transcriptome alterations in S. aureus strain ATCC29213 treated with telavancin for 15 min and 60 min in comparing with other agents treatment, including vancomycin, enduracidin, m-chlorophenylhydrazone. MHB cultures (biological replicates: N=3) were then grown to exponential phase (OD580=0.35) before the addition of telavancin(8 M-BM-5g/ml final concentration), or vancomycin (10 /M-BM-5g ml) or CCCP (2 M-BM-5g/ ml ); or enduracidin (1 M-BM-5g ml) and incubated for an additional 15 min , and 60 min before sampling. Dye-swapping was performed between samples.
2012-04-13 | E-GEOD-37272 | biostudies-arrayexpress
Project description:Coordinated protein-coding sequence transcriptional responses of Staphylococcus aureus to antimicrobial exposure are well described but little is known of the role of bacterial non-coding, small RNAs (sRNAs) in these responses. Here we used RNAseq to investigate the sRNA response of the epidemic multiresistant hospital ST239 S. Aureus strain JKD6009 and its vancomycin-intermediate clinical derivative, JKD6008, after exposure to four antibiotics representing the major classes of antimicrobials used to treat methicillin-resistant S. Aureus infections. These agents included vancomycin, linezolid, ceftobiprole, and tigecycline. We identified 410 potential sRNAs (sRNAs) and then compared global sRNA and mRNA expression profiles at 2 and 6 hours, without antibiotic exposure, and after exposure to 0.5 x MIC for each antibiotic, for both JKD6009 (VSSA), and JKD6008 (VISA). Two strains were used (JKD6009, vancomycin-susceptible S. Aureus; JKD6008, in vivo derived vancomycin-intermediate S. Aureus). The complete JKD6008 genome seqeuce was used as the reference. Two time points, 2 hours and 6 hours after culture in Mueller Hinton broth. Strains were exposed to no antibiotic, or 0.5 x MIC for 10 mins for the following antibiotics; vancomycin, linezolid, ceftobiprole, tigecycline. RNA isolation procedures enriched for mRNA or sRNA. The 40 cDNA libraries were sequenced using a whole flowcell (8 lanes) in an Illumina genome analyzer GAII for 36 cycles. Data was analyzed using the BioConductor package limma, and by applying non-negative matrix factorization to determine the impact of antibiotic exposure on the sRNA and mRNA transcriptional profiles.
2013-06-10 | E-GEOD-40864 | biostudies-arrayexpress
Project description:Complete reconstitution of the vancomycin-intermediate Staphylococcus aureus (VISA) phenotype of Mu50 was achieved by sequentially introducing mutations into five genes of a vancomycin-susceptible S. aureus (VSSA) strain ∆IP. Introduction of mutation Ser329Leu into vraS encoding the sensor histidine kinase of vraSR two-component regulatory (TCR) system and another mutation Glu146Lys into msrR, encoding putative methionine sulfoxide reductase regulator, raised vancomycin resistance to the level of heterogeneously vancomycin-intermediate S. aureus (hVISA) strain Mu3. Introduction of two more mutations, graR (Asn197Ser) of graSR TCR system and rpoB(His481Tyr) encoding ß subunit of RNA polymerase, converted the hVISA strain into a VISA strain having the level of vancomycin resistance of Mu50. Surprisingly, however, the constructed quadruple mutant strain did not have thickened cell wall, a cardinal feature of VISA phenotype. Subsequent study showed that cell-wall thickening was an inducible phenotype with the mutant strain as opposed to that of Mu50, which is a constitutive one. Finally, introduction of mutation Ala297Val into the orf SAV2309 of the mutant strain converted the inducible cell-wall thickening into a constitutive one. SAV2309 encodes a putative formate dehydrogenase (designated Fdh2). Though not a transcription regulator, the mutation of the fdh2 caused a significant change in transcriptome. Thus, all of the five mutated genes required for VISA phenotype acquisition were directly or indirectly involved in the regulation of cell physiology. VISA seemed to be achieved through multiple genetic events accompanying drastic changes in cell physiology.
2016-04-19 | GSE43643 | GEO
Project description:To determine if significant genomic changes are associated with the development of vancomycin intermediate Staphylococcus aureus, genomic DNA microarrays were performed to compare the initial vancomycin susceptible Staphylococcus aureus (VSSA) and a related vancomycin intermediate Staphylococcus aureus (VISA) isolate from five unique patients (five isolate pairs). Keywords: comparative genomic hybridization
2006-11-03 | GSE5047 | GEO
Project description:hVISA clinical strain Mu3 spontaneously generates VISA at an extremely high frequency (1x10-6 or greater) within its cell population. The VISA-converted mutant strains generally grow slower than their parent hVISA strain, but they usually form colonies on vancomycin-containing agar plates after 48 hours of incubation on population analysis. However, we noticed a curious group of VISA mutants whose colony formation is much more delayed and observed as discrete colonies only after 96 hours incubation. They have extremely prolonged lag-phase and doubling-times, but recorded vancomycin MICs of 8 to 24 mg/L when determined after 48 to 96 hours of incubation. We established strain Mu3-6RS having vancomycin MIC of 12 mg/L (at 72h) as a representative of the ‘slow VISA’ (sVISA) strains. Its cell wall was thickened, and autolytic activity was decreased as compared with those of the parent strain Mu3. Whole genome sequencing of Mu3-6RS revealed only one mutation, which substituted the 512th amino-acid sequence of RNA polymerase ß-subunit from Arg of Mu3 to Proline. Its VISA phenotype was unstable, and the strain frequently reverted to hVISA with concomitant loss of small colony morphology, cell-wall thickness and reduced autolytic activity. Sequencing of rpoB genes of the reverted strains revealed mutations affecting the 512th codon replacing the Proline of Mu3-6RS to Leucine, Serine, or Histidine. This study proposes sVISA as a discrete class of VISA phenotype, which can serve as a temporary shelter for S. aureus to survive relatively high concentrations of vancomycin. The sVISA spontaneously returns to hVISA when the threat of vancomycin passes by. The rpoB(R512P) mutation may be regarded as a ‘regulatory mutation’ switching on and off the reversible sVISA phenotype.
2014-03-31 | GSE50826 | GEO
Project description:Staphylococcus aureus is a notorious bacterial pathogen that causes a broad range of human diseases, and isolates that are resistant to several antibiotic classes including last resort antibiotics like vancomycin and daptomycin complicate the situation. We characterized S. aureus VC40, a strain that shows full resistance to vancomycin (MIC of 64 M-BM-5g/ml) and daptomycin (MIC of 4 M-BM-5g/ml) as well as a decreased susceptibility to further cell wall active agents. Genome sequencing revealed mutations in genes encoding the histidine kinases WalK and VraS that control cell envelope related processes and gene expression profiling indicated the induction of the respective regulons in strain VC40. Reconstitution of the mutations in walK or vraS into the susceptible S. aureus NCTC 8325 background resulted in a considerably increased resistance to vancomycin and daptomycin with MICs surpassing the clinical breakpoints for these antibiotics, thereby generating vancomycin-intermediate S. aureus (VISA) strains. As observed for S. aureus VC40, the walKwalk and vraS mutations also led to an increased expression of the respective regulons in the NCTC 8325 background. Phenotypic studies showed that S. aureus VC40 as well as the walKwalk and vraS mutants of strain NCTC 8325 were characterized by a significantly thickened cell wall, a decreased growth rate, a reduced autolytic activity and an increased resistance to lysostaphin-induced lysis. These results demonstrate that the WalK and VraS histidine kinases act as major switches which allow S. aureus to rapidly develop vancomycin resistance up to the VISA level via mutation of one single gene locus and concomitantly contribute to cross-resistance to other antibiotics including the last resort antibiotic daptomycin. Microarray was used to evaluate alteration in the transcriptome of mutS mutant and compared to the parental strain VC40
2014-08-18 | E-GEOD-46887 | biostudies-arrayexpress
Project description:hVISA clinical strain Mu3 spontaneously generates VISA at an extremely high frequency (1x10-6 or greater) within its cell population. The VISA-converted mutant strains generally grow slower than their parent hVISA strain, but they usually form colonies on vancomycin-containing agar plates after 48 hours of incubation on population analysis. However, we noticed a curious group of VISA mutants whose colony formation is much more delayed and observed as discrete colonies only after 96 hours incubation. They have extremely prolonged lag-phase and doubling-times, but recorded vancomycin MICs of 8 to 24 mg/L when determined after 48 to 96 hours of incubation. We established strain Mu3-6RS having vancomycin MIC of 12 mg/L (at 72h) as a representative of the M-bM-^@M-^Xslow VISAM-bM-^@M-^Y (sVISA) strains. Its cell wall was thickened, and autolytic activity was decreased as compared with those of the parent strain Mu3. Whole genome sequencing of Mu3-6RS revealed only one mutation, which substituted the 512th amino-acid sequence of RNA polymerase M-CM-^_-subunit from Arg of Mu3 to Proline. Its VISA phenotype was unstable, and the strain frequently reverted to hVISA with concomitant loss of small colony morphology, cell-wall thickness and reduced autolytic activity. Sequencing of rpoB genes of the reverted strains revealed mutations affecting the 512th codon replacing the Proline of Mu3-6RS to Leucine, Serine, or Histidine. This study proposes sVISA as a discrete class of VISA phenotype, which can serve as a temporary shelter for S. aureus to survive relatively high concentrations of vancomycin. The sVISA spontaneously returns to hVISA when the threat of vancomycin passes by. The rpoB(R512P) mutation may be regarded as a M-bM-^@M-^Xregulatory mutationM-bM-^@M-^Y switching on and off the reversible sVISA phenotype. 5 sample analysis using 60mer-oligo microarray, 3 rpoB mutant(R512P,R512L,R512S), 2 wild-type strain(Mu3, M-NM-^TIP)
2014-03-31 | E-GEOD-50826 | biostudies-arrayexpress
Project description:Staphylococcus aureus is a notorious bacterial pathogen that causes a broad range of human diseases, and isolates that are resistant to several antibiotic classes including last resort antibiotics like vancomycin and daptomycin complicate the situation. We characterized S. aureus VC40, a strain that shows full resistance to vancomycin (MIC of 64 µg/ml) and daptomycin (MIC of 4 µg/ml) as well as a decreased susceptibility to further cell wall active agents. Genome sequencing revealed mutations in genes encoding the histidine kinases WalK and VraS that control cell envelope related processes and gene expression profiling indicated the induction of the respective regulons in strain VC40. Reconstitution of the mutations in walK or vraS into the susceptible S. aureus NCTC 8325 background resulted in a considerably increased resistance to vancomycin and daptomycin with MICs surpassing the clinical breakpoints for these antibiotics, thereby generating vancomycin-intermediate S. aureus (VISA) strains. As observed for S. aureus VC40, the walKwalk and vraS mutations also led to an increased expression of the respective regulons in the NCTC 8325 background. Phenotypic studies showed that S. aureus VC40 as well as the walKwalk and vraS mutants of strain NCTC 8325 were characterized by a significantly thickened cell wall, a decreased growth rate, a reduced autolytic activity and an increased resistance to lysostaphin-induced lysis. These results demonstrate that the WalK and VraS histidine kinases act as major switches which allow S. aureus to rapidly develop vancomycin resistance up to the VISA level via mutation of one single gene locus and concomitantly contribute to cross-resistance to other antibiotics including the last resort antibiotic daptomycin.
2014-08-18 | GSE46887 | GEO
Project description:This is a repository of LC/MS, HPLC, BPC data collected from two strains of Staphylococcus aureus: Strain D592 grown in RPMI (+10%LB) and CA-MHB, and strain D712 grown in RPMI (+10%LB) and CA-MHB. Both stains in both media conditions were grown in both the presence and absence of vancomycin.
2020-05-01 | MSV000085358 | GNPS