Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1215779 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR32129069.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 1 of 1 |
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Project description:Pathogen sequencing information of a Pulmonary Tuberculosis patient
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Project description:Pulmonary tuberculosis is a multigene disease, and some of the genes affect the development of Pulmonary tuberculosis. The study wants to find different expression genes in blood from Pulmonary tuberculosis patient and normal people who have genetic relationship wtih each other. We used microarrays to detail the global programme of gene expression in the blood between Pulmonary tuberculosis patient's and normal people's who have genetic relationship wtih each other.
2017-12-06 | GSE107731 | GEO
Project description:Tuberculosis (TB) is difficult to diagnose under complex clinical conditions. Exosomal miRNAs have emerged as promising disease biomarkers. We aim to investigate the potential of exosomal miRNAs to assist with TB clinical diagnosis. In the present research, we used the Affymetrix Genechip miRNA 4.0 Array to investgate the profiles of differentially expressed miRNAs (DEMs) in the exosomes of peripheral blood plasma. As a result, exosomal miRNA profiling yielded a total of 102 DEMs (98 with up-expression and 4 with down-expression) between the TB (pulmonary tuberculosis and tuberculosis meningitis) patients and controls.
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Project description:We used human miRNA arrays to explore the miRNA expression profile in pulmonary tuberculosis patients (PTB), pulmonary with pleural tuberculosis patients (PPLTB) and non-tuberculous pleurisy patients (NTP).
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Project description:Fresh resected lung tissues were obtained from nine tuberculosis patients with elevated pulmonary 18F-FDG avidity. Lung tissues with 18F-FDG avidity and nearby uninvolved tissues were profiled with miRNA sequencing.
2025-04-09 | GSE276819 | GEO
Project description:Understanding the immune response to tuberculosis requires greater knowledge of humoral responses. To characterize antibody targets and the effect of disease parameters on target recognition, we developed a systems immunology approach that integrated detection of antibodies against the entire Mycobacterium tuberculosis proteome, bacterial metabolic and regulatory pathway information, and patient data. Probing ~4,000 M. tuberculosis proteins with sera from >500 suspected tuberculosis patients worldwide revealed that antibody responses recognized ~10% of the bacterial proteome. This result defines the immunoproteome of M. tuberculosis, which is rich in membrane-associated and extracellular proteins. Most serum reactivity during active tuberculosis focused onto ~0.5% of the proteome. Within this pool, which is selectively enriched for extracellular proteins (but not for membrane-associated proteins), relative target preference varied among patients. The shift in relative M. tuberculosis protein reactivity observed with active tuberculosis defines the evolution of the humoral immune response during M. tuberculosis infection and disease. Peripheral blood was collected from prospectively enrolled TB suspects among subjects seeking care for pulmonary symptoms at clinics associated with national TB control programs in 11 countries. M. tuberculosis proteome microarrays representing 4099 bacterial protein spots were probed with sera from 561 TB suspects. Based on the final diagnosis, they belonged to two classes: TB (n=254) and Non-TB Disease (n=307). In addition, healthy individuals negative to Latent TB Infection (LTBI neg, n=64) were also tested (negative control sera). Each serum was tested with a single array and no replicate experiments were performed. The reactivity of a serum to an M. tuberculosis protein (reactivity call) was defined based on the distribution of negative control sera intensity for that protein using Z-statistics. Based on the distribution of reactivity calls, 27 outlier samples reacting with more than 20 proteins were excluded from further analysis. The association of reactivity calls of each protein with TB/NTBD status of TB suspects was determined by estimating odds ratio and 95% confidence interval.
2010-07-13 | E-GEOD-19433 | biostudies-arrayexpress
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Project description:The W-Beijing family of Mycobacterium tuberculosis (Mtb) strains is known for its high-prevalence and -virulence, as well as for its genetic diversity, as recently reported by our laboratories and others. However, little is known about how the immune system responds to these strains. To explore this issue, here we used reverse engineering and genome-wide expression profiling of human macrophage-like THP-1 cells infected by different Mtb strains of the W-Beijing family, as well as by the reference laboratory strain H37Rv. Detailed data mining revealed that host cell transcriptome responses to H37Rv and to different strains of the W-Beijing family are similar and overwhelmingly induced during Mtb infections, collectively typifying a robust gene expression signature ("THP1r2Mtb-induced signature"). Analysis of the putative transcription factor binding sites in promoter regions of genes in this signature identified several key regulators, namely STATs, IRF-1, IRF-7, and Oct-1, commonly involved in interferon-related immune responses. The THP1r2Mtb-induced signature appeared to be highly relevant to the interferon-inducible signature recently reported in active pulmonary tuberculosis patients, as revealed by cross-signature and cross-module comparisons. Further analysis of the publicly available transcriptome data from human patients showed that the signature appears to be relevant to active pulmonary tuberculosis patients and their clinical therapy, and be tuberculosis specific. Thus, our results provide an additional layer of information at the transcriptome level on mechanisms involved in host macrophage response to Mtb, which may also implicate the robustness of the cellular defense system that can effectively fight against genetic heterogeneity in this pathogen.
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Project description:Mycobacterium tuberculosis is a facultative intracellular pathogen, responsible for causing tuberculosis. The harsh environment in which M. tuberculosis survives requires this pathogen to maintain an evolutionary advantage. However, the apparent absence of horizontal gene transfer in M. tuberculosis imposes restrictions in the ways by which evolution can occur. Large scale changes in the genome can be introduced through genome reduction, recombination events and structural variation. Here, we identify a functional chimeric protein in the ppe38-71 locus, the absence of which is known to have an impact on protein secretion and virulence. To examine whether this approach was used more often by this pathogen we further develop software that detects potential gene fusion events from multigene deletions using whole-genome sequencing data. With this software we could identify a number of other putative gene-fusion events within the genomes of M. tuberculosis isolates. We were able to demonstrate the expression of one of these gene fusions at the protein level using mass spectrometry. Therefore, gene fusions may provide an additional means of evolution for M. tuberculosis in its natural environment whereby novel proteins and functions can arise.
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Project description:To understand the host-pathogen association by determining the patient SNPs associated with Mycobacterium tuberculosis genotypes in the Ugandan population. by analysing the relationship between the SNPs and different Mtb genotypes, the study seeks to explain why the Mtb Ugandan genotype is prevalent in Uganda and uncover host pathogen related therapies towards that are increasing being discussed as possible adjunct treatments for tuberculosis.
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