Mycobacterium tuberculosis subsp. tuberculosis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1135144 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:WGS of MTB (Astana 2014)
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Project description:In-vivo Gene Signatures of Mycobacterium tuberculosis In C3HeB/FeJ Mice In this experiment we have compared Mtb transcriptomics in-vivo, using samples derived from chronically infected C3HeB/FeJ mice, which produce human like caseating lesions, unlike other murine species, to Mtb cultured in-vitro. Similarly, the genome-wide expression of MtbdeldosR, MtbdeldosS and MtbdeldosT mutants is also compared between lungs from C3HeB/FeJ mice and in-vitro culturing.
2015-07-11 | E-GEOD-70765 | biostudies-arrayexpress
Project description:MDR and XDR tuberculosis tested with WGS and Xpert MTB/XDR
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Project description:The overall goal of the project is to identify candidate biomarkers of Active infection with Mycobacterium tuberculosis (Mtb) in individuals with or without HIV. Samples were analyzed from two tuberculosis (TB) endemic countries, Brazil and South Africa (SA), as well as from the United States (US). The US site included patients that were in the early stages of Active TB, with mean symptom duration of 1.5 months. The subjects from the Brazil site had mean symptom duration of 6 months, and the SA site subjects had advanced TB. All sites also provided samples asymptomatic for TB or with Latent TB infection. The US and SA sites also had subjects with and without HIV co-infection, whereas the Brazilian subjects were all HIV-. This specific dataset corresponds to the Discovery step of the study, for the US center.
2019-11-22 | PXD000517 | Pride
Project description:The purpose of this study was to identify Mtb- and hsa-encoded miRNAs produced in infected macrophages. RNA from 9 THP-1 samples (3 were uninfected, 3 were infected with Mtb H37Rv for 3 days and 3 were infected with Mtb H37Rv for 6 days) was sequenced and miRNAs were detected.
2020-02-24 | GSE145770 | GEO
Project description:Mycobacterium tuberculosis (Mtb) cultured in the absence of detergent forms biofilm-like cords, a clinical identifier of virulence. Using lung-on-chip and mouse infection models, we show that cord growth in alveolar cells contributes to the suppression of innate immune signalling via nuclear compression. Thereafter, extracellular cords cause contact-dependent phagocyte death but grow intercellularly between epithelial cells. These “mechanopathological” mechanisms explain the greater proportion of alveolar lesions with increased immune infiltration and dissemination defects in cording-deficient Mtb infections. Compression of WT Mtb lipid monolayers induces a phase transition that enables mechanical energy storage. Agent-based simulations demonstrate that the increased energy storage capacity is sufficient for the formation of stable cords that maintain structural integrity despite mechanical perturbation. Moreover, bacteria in cords remain translationally active despite prolonged antibiotic exposure and regrow rapidly upon cessation of treatment. This study provides a conceptual framework for the biophysics of cord architectures and their functional roles in tuberculosis infection and therapy, independent of mechanisms ascribed to single bacteria.
2023-11-01 | GSE238102 | GEO
Project description:A cell-based phenotypic screen for inhibitors of biofilm formation in Mycobacterium tuberculosis (Mtb) identified the small molecule TCA1, which has bactericidal activity against both drug susceptible and drug resistant Mtb, and synergizes with rifampicin (RIF) or isoniazid (INH) in sterilization of Mtb in vitro. In addition, TCA1 has bactericidal activity against non-replicating Mtb in vitro and is efficacious in acute and chronic Mtb infection mouse models, both alone and in combination with INH or RIF. Transcriptional analysis revealed that TCA1 down-regulates genes known to be involved in Mtb dormancy and drug tolerance. Mutagenesis and affinity-based methods identified DprE1 and MoeW, enzymes involved in cell wall and molybdenum cofactor biosynthesis, respectively, as the targets responsible for TCA1’s activity. These in vitro and in vivo results indicate that TCA1functions by a novel mechanism and suggest that it may be the first product of a promising new approach for the development of anti-tuberculosis drugs.
2013-05-24 | GSE42151 | GEO
Project description:A cell-based phenotypic screen for inhibitors of biofilm formation in Mycobacterium tuberculosis (Mtb) identified the small molecule TCA1, which has bactericidal activity against both drug susceptible and drug resistant Mtb, and synergizes with rifampicin (RIF) or isoniazid (INH) in sterilization of Mtb in vitro. In addition, TCA1 has bactericidal activity against non-replicating Mtb in vitro and is efficacious in acute and chronic Mtb infection mouse models, both alone and in combination with INH or RIF. Transcriptional analysis revealed that TCA1 down-regulates genes known to be involved in Mtb dormancy and drug tolerance. Mutagenesis and affinity-based methods identified DprE1 and MoeW, enzymes involved in cell wall and molybdenum cofactor biosynthesis, respectively, as the targets responsible for TCA1M-bM-^@M-^Ys activity. These in vitro and in vivo results indicate that TCA1functions by a novel mechanism and suggest that it may be the first product of a promising new approach for the development of anti-tuberculosis drugs. Transcriptional profile of TCA1-treated cells relative to DMSO-treated control. Three biological replicates, third is a dye flip.
2013-05-24 | E-GEOD-42151 | biostudies-arrayexpress
Project description:Surface shaving Mtb using two concentrations of trypsin: 0.4 ug/mL and 0.05 ug/mL. Both bacteria and supernatant without the bacteria were subject to trypsinization, to allow for a ratio between samples to identify candidate surface proteins.
2024-12-11 | PXD052936 | Pride
Project description:Diverse chemical modifications fine-tune the function and metabolism of tRNA. Although tRNA modification is universal in all kingdoms of life, profiles of modifications, their functions, and physiological roles have not been elucidated in most organisms including the human pathogen, Mycobacterium tuberculosis (Mtb), the causative agent of tuberculosis. To identify physiologically important modifications, we surveyed the tRNA of Mtb, using tRNA sequencing (tRNA-seq). Reverse transcription-derived error signatures in tRNA-seq predicted the sites and presence of 9 modifications. Several chemical treatments prior to tRNA-seq expanded the number of predictable modifications. Deletion of Mtb genes encoding two modifying enzymes, TruB and MnmA, eliminated their respective tRNA modifications, validating the presence of modified sites in tRNA species.
2023-08-11 | GSE240200 | GEO