Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1040214 | ENA |
REPOSITORIES: ENA
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Project description:The challenge in treating tuberculosis (TB) associated with drug resistance and toxicity drives the efforts in the development of alternative strategies to combat Mycobacterium tuberculosis (Mtb), a major causative pathogen in humans. Propolis extract is considered a promising therapeutic agent since the findings on its effective functions against Mtb.
2025-11-26 | PXD058274 | JPOST Repository
Project description:11 Mycobacterium tuberculosis mutants resistant to D-cycloserine were isolated in the laboratory. Genomic DNA was isolated and whole genomes were sequenced to perform SNP calling and identify possible mutations associated with resistance.
2018-12-28 | E-MTAB-5935 | biostudies-arrayexpress
Project description:Analysis of Metfromin induced changes in the lung cells of Mycobacterium tuberculosis infected mouse at gene expression level. The hypothesis tested in the present study was whether metformin has any effect on the host immune response in Mycobacterium tuberculosis infected mice? Results provide important information on the effect of metformin on the inflammatory response and immune activation associated with mycobacterial infection. In conclusion, Metfromin normalizes the chronic inflammation associated with Mycobacterium tuberculosis infection.
2014-12-02 | GSE57275 | GEO
Project description:The innate immune system provides the first response to pathogen infection and orchestrates the activation of the adaptive immune system. Though a large component of the innate immune response is common to all infections, pathogen-specific innate immune responses have been documented as well. The innate immune response is thought to be especially critical for fighting infection with Mycobacterium tuberculosis (MTB), the causative agent of tuberculosis (TB). While TB can be a deadly disease, only 5-10% of individuals infected with MTB develop active disease, and this inter-individual variation is, at least partly, heritable. Studies of inter-individual variation in the innate immune response to MTB infection may therefore shed light on the genetic basis for variation in susceptibility to TB. Yet, to date, we still do not know which properties of the innate immune response are specific to MTB infection and which represent a general response to pathogen infection. To begin addressing this gap, we infected macrophages with eight different bacterial pathogens, including different MTB strains and related mycobacteria, and studied the transcriptional response to infection. We found that although the gene expression changes were largely consistent across the bacterial infection treatments, we were able to identify a novel subset of genes whose regulation was affected specifically by infection with mycobacteria. Genetic variants that are associated with regulatory differences in these genes should be considered candidate loci for explaining inter-individual susceptibility TB. RNA-seq of monocyte-derived macrophages isolated from 6 healthy European males at 4, 18, and 48 hours post-infection with the following 8 bacteria: Mycobacterium tuberculosis (MTB) H37Rv, Mycobacterium tuberculosis GC1237, MTB GC1237, bacillus Calmette-Guérin (BCG), Mycobacterium smegmatis, Yersinia pseudotuberculosis, Salmonella typhimurium, and Staphylococcus epidermidis. table-s1.txt is a tab-delimited text file that contains the batch-corrected log2 counts per million for each of the 156 samples, as well as the Ensembl gene ID and gene name. BCG = bacillus Calmette-Guérin GC = Mycobacterium tuberculosis GC1237 Rv = Mycobacterium tuberculosis (MTB) H37Rv Rv+ = heat-inactivated MTB H37Rv Salm = Salmonella typhimurium Smeg = Mycobacterium smegmatis Staph = Staphylococcus epidermidis Yers = Yersinia pseudotuberculosis
2015-03-31 | E-GEOD-67427 | biostudies-arrayexpress
Project description:The cytokine IL-10 deactivates macrophages and has been shown to impair resistance to mycobacterial infection. We have infected transgenic mice overexpressing IL-10 under control of the macrophage-specific CD68 promoter (macIL-10tg mice) with Mycobacterium tuberculosis by aerosol and found increased bacterial loads in the lungs of macIL-10tg mice. To identify programs of genes regulated by IL-10 and associated with increased mycobacterial replication, genome-wide expression analysis was performed. Experiment Overall Design: Impact of IL-10 pulmonary gene expression in mouse M. tuberculosis infection
2009-01-17 | E-GEOD-14316 | 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. 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:Identification of genetic polymorphisms associated with inter-individual variation in immune response to Mycobacterium tuberculosis infection.
2011-12-30 | GSE34588 | GEO
Project description:Next-gen sequencing has facilitated studies of bacterial genomes and uncovered pathogen variants associated with clinically relevant phenotypes such as antibiotic resistance. However, these studies are primarily focused on bacteria cultured from patient tissues, and thus, viable but non-cultivable bacteria are not assessed. This yields an incomplete genetic state of bacteria during infection. Nevertheless, it is possible to capture bacterial transcripts in libraries designed to amplify eukaryotic mRNA. These reads are often considered spurious or nuisance and are rarely investigated. Here we demonstrate that Mycobacterium tuberculosis (Mtb) ribosomal RNA sequences are detected in host human cells obtained from peripheral lymph node aspirates from patients infected with Mtb.
2025-03-04 | GSE281835 | GEO
Project description:Mycobacterium tuberculosis Resistance Ecuador
| PRJNA827129 | ENA
Project description:During Mycobacterium tuberculosis infections bacteria are engulfed by macrophages, a main line of defense against invading pathogens. Upon activation, macrophages increase glycolysis producing the antibacterial aldehyde methylglyoxal. To test if bacterial methylglyoxal resistance is required for robust infections, we sought to identify Mycobacterium tuberculosis defense mechanisms against methylglyoxal. We identified phoP mutants were among the most highly sensitive strains to methylglyoxal in vitro. phoP mutants are attenuated in mice but were even more attenuated in mice that accumulate methylglyoxal. We further found phoP bacilli exhibited increased membrane permeability and were more permeable to methylglyoxal. Suppressor mutations in the fatty acid Beta-oxidation genes fadE25 or fixB restored impermeability and resistance to methylglyoxal to a phoP mutant. Together, our data show that a major virulence role for PhoP is to provide Mycobacterium tuberculosis resistance to methylglyoxal toxicity in vivo by regulating cell envelope integrity. The mass spectrometry files supporting this hypothesis are deposited here.
2025-08-07 | MSV000098760 | MassIVE