Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1066082 | ENA |
REPOSITORIES: ENA
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Project description:The emergence of drug resistance among tuberculosis (TB) patients is often associated with their non-compliance to the length of the chemotherapy, which can reach up to 2 years for the treatment of multi-drug-resistant (MDR) TB. Drugs that would kill TB faster and would not lead to the development of drug resistance could shorten chemotherapy significantly. In Escherichia coli, the common mechanism of cell death by bactericidal antibiotics is the generation of highly reactive hydroxyl radicals via the Fenton reaction. Since ascorbic acid (vitamin C) is known to drive the Fenton reaction, we tested whether the Fenton reaction could lead to a bactericidal event in Mycobacterium tuberculosis by treating M. tuberculosis cultures with vitamin C. Here, we report that the addition of vitamin C to drug-susceptible, MDR and extensively drug-resistant (XDR) M. tuberculosis strains results in sterilization of the cultures in vitro. We show that the sterilizing effect of vitamin C on M. tuberculosis was dependent on the production of high ferrous ion levels and reactive oxygen species. Although, this potent sterilizing activity of vitamin C against M. tuberculosis in vitro was not observed in mice, we believe this activity needs further investigation. Comparison of vitamin C treated Mycobacterium tuberculosis transcriptome relative to untreated; Three biological replicates, second is a dye flip
2013-05-24 | E-GEOD-42293 | biostudies-arrayexpress
Project description:The emergence of drug resistance among tuberculosis (TB) patients is often associated with their non-compliance to the length of the chemotherapy, which can reach up to 2 years for the treatment of multi-drug-resistant (MDR) TB. Drugs that would kill TB faster and would not lead to the development of drug resistance could shorten chemotherapy significantly. In Escherichia coli, the common mechanism of cell death by bactericidal antibiotics is the generation of highly reactive hydroxyl radicals via the Fenton reaction. Since ascorbic acid (vitamin C) is known to drive the Fenton reaction, we tested whether the Fenton reaction could lead to a bactericidal event in Mycobacterium tuberculosis by treating M. tuberculosis cultures with vitamin C. Here, we report that the addition of vitamin C to drug-susceptible, MDR and extensively drug-resistant (XDR) M. tuberculosis strains results in sterilization of the cultures in vitro. We show that the sterilizing effect of vitamin C on M. tuberculosis was dependent on the production of high ferrous ion levels and reactive oxygen species. Although, this potent sterilizing activity of vitamin C against M. tuberculosis in vitro was not observed in mice, we believe this activity needs further investigation.
2013-05-24 | GSE42293 | GEO
Project description:Background: This study aimed to explore potential tobramycin-resistant mutagenesis of Escherichia coli (E. coli) strains after spaceflight. Methods: A spaceflight-induced mutagenesis of multi-drug resistant E.coli strain (T1_13) on the outer space for 64 days (ST5), and a ground laboratory with the same conditions (GT5) were conducted. Both whole-genome sequencing and RNA-sequencing were performed. Results: A total of 75 SNPs and 20 InDels were found to be associated with the resistance mechanism. Compared to T1_13, 1242 genes were differentially expressed in more than 20 of 38 tobramycin-resistant E. coli isolates while not in GT5. Function annotation of these SNPs/InDels related genes and differentially expressed genes was performed. Conclusion: This study provided clues for potential tobramycin-resistant spaceflight-induced mutagenesis of E. coli.
2019-12-13 | GSE123795 | GEO
Project description:We examined the microRNA profiles of THP-1 macrophages upon the MTB infection of (1) Beijing/W and non-Beijing/W clinical strains, and (2) susceptible and multidrug-resistant (MDR-) MTB strains. THP-1 cells were induced differentiation into a macrophage phenotype. Then cells were infected with three MDR (INHR, RIFR) Beijing/W, three sensitive (INHS, RIFS) Beijing/W, three MDR(INHR, RIFR) non-Beijing/W, and three sensitive (INHS, RIFS) non-Beijing/W strains. Total RNA were extracted and transfered into cDNA for miRNA profile analysis. Non-infected cells were used as control.
2015-07-01 | E-GEOD-65811 | biostudies-arrayexpress
Project description:Efforts to eradicate TB are largely threatened by drug-resistant tuberculosis, particularly, multidrug-resistant tuberculosis (MDR-TB). It is imperative to find one or more specific biomarkers for diagnosing MDR-TB earlier and declining the incidence. Growing evidences have showed lncRNAs are widely expressed and take part in the genesis and development of many diseases, including tuberculosis. Therefore, to screen the differential lncRNAs among MDR-TB, drug-sensitive tuberculosis(DS-TB) and healthy controls(HCs) is a good strategy to acquire potential biomarkers for MDR-TB diagnosis and partly describe the mechanism of MDR-TB. Here, the present study aimed to investigate the differential expression profile of lncRNAs in serum among patients with MDR-TB ,DS-TB and HCs using lncRNA microarray
2021-09-10 | GSE183787 | GEO
Project description:The emergence of multidrug resistant (MDR) Mycobacterium tuberculosis (Mtb) strains, resistant to the frontline anti-tubercular drugs rifampicin and isoniazid, forces treatment with less effective and toxic second-line drugs and stands to derail TB control efforts. However, the immune response to MDR Mtb infection remains poorly understood. Here, we determined the RNA transcriptional profile of in vitro generated macrophages to infection with either drug susceptible Mtb HN878 or MDR Mtb W_7642 infection.
2018-12-26 | GSE115495 | GEO
Project description:Gene expression profiles were assessed for vincristine-sensitive parental ovarian tumor cell line (SKOV3) and its highly vincristine-resistant derivative (SKVCR 2.0) Keywords: vincristine, drug resistance, ovarian, SKOV3, MDR
2007-08-24 | GSE7556 | GEO
Project description:Metformin is the therapy of choice for treating type 2 diabetes and is currently repurposed for a wide range of diseases including aging. Recent evidence implicates the gut microbiota as a site of metformin action. Combining two tractable genetic models, the bacterium E. coli and the nematode C. elegans, we performed C. elegans RNAseq to investigate the role of the metformin sensitive OP50 and metformin resistant OP50-MR E. coli microbiota in the drug effects on the host. Our data suggest an evolutionarily conserved bacterial mediation of metformin effects on host lipid metabolism and lifespan.
2019-07-13 | E-MTAB-7272 | biostudies-arrayexpress