Rv0495c mediated host response
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB64000 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Define genes expressed by CD4 T cells in the lungs of Mycobacterium tuberculosis-infected mice
2023-11-06 | GSE235563 | GEO
Project description:To investigate the role of LDHA in myeloid cells in the response to pulmonary infection with Mycobacterium tuberculosis, we infected LDHAfl/fl:LysM+/- mice with Mtb-H37Rv via the aerosol route. We then performed gene expression profiling analysis using data obtained from RNA-seq of the lungs of these animals at 4 and 30 weeks post infection.
2023-08-09 | GSE234115 | GEO
Project description:Highly pathogenic avian influenza virus (HPAIV) is a permanent threat due to its capacity to cross species barriers and generate severe infections and high mortality in humans. Recent findings have highlighted the potential role of PB1-F2, a small accessory influenza protein, in the pathogenesis process mediated by HPAIV in mammals. In this study, using a recombinant H5N1 HPAIV (wt) and its PB1-F2-deleted mutant (M-NM-^TF2), we studied the effects of PB1-F2 in a chicken model. Unexpectedly, when using low inoculation dose we observed that the wt-infected chickens had a higher survival rate than the M-NM-^TF2-infected chickens, a feature that contrasts with what is usually observed in mammals. High inoculation dose had similar mortality rate for both viruses, and comparison of the bio-distribution of the two viruses indicated that the expression of PB1-F2 allows a better spreading of the virus within chicken embryos. Transcriptomic profiles of lungs and blood cells were characterized at two days post-infection in chickens inoculated with the wild type (wt) or the M-NM-^TF2 mutant viruses. In lungs, the expression of PB1-F2 during the infection induced pathways related to calcium signaling and repressed a large panel of immunological functions. In blood cells, PB1-F2 was associated to a gene signature specific for mitochondrial dysfunction and down-modulated leucocytes activation. Finally we compared the effect of PB1-F2 in lungs of chickens and mice. We identified that gene signature associated to tissue damages is a PB1-F2 feature shared by the two species; by contrast, the early inhibition of immune response mediated by PB1-F2 observed in chickens is not seen in mice. In summary, our data suggest that PB1-F2 expression deeply affect the immune host response in chickens in a way that may attenuate pathogenicity, a feature differing from what was previously observed in mammal species. Three-condition experiment, virus-infected (wt or M-NM-^TF2) vs. Mock-infected chickens. Biological replicates: 2x5 control replicates, 5 wt replicates, 5 M-NM-^TF2 replicates.
2014-09-01 | E-GEOD-56506 | biostudies-arrayexpress
Project description:Define genes differentially expressed by Nur77-GFP HI and LO CD4 T cells FACS sorted from the lungs of Mycobacterium tuberculosis-infected mice
2023-11-06 | GSE235799 | GEO
Project description:Define genes differentially expressed by Nur77-GFP HI and LO CD4 T cells FACS sorted from the lungs of Mycobacterium tuberculosis-infected mice with bulk RNA seq
2023-11-06 | GSE235564 | GEO
Project description:Highly pathogenic avian influenza virus (HPAIV) is a permanent threat due to its capacity to cross species barriers and generate severe infections and high mortality in humans. Recent findings have highlighted the potential role of PB1-F2, a small accessory influenza protein, in the pathogenesis process mediated by HPAIV in mammals. In this study, using a recombinant H5N1 HPAIV (wt) and its PB1-F2-deleted mutant (ΔF2), we studied the effects of PB1-F2 in a chicken model. Unexpectedly, when using low inoculation dose we observed that the wt-infected chickens had a higher survival rate than the ΔF2-infected chickens, a feature that contrasts with what is usually observed in mammals. High inoculation dose had similar mortality rate for both viruses, and comparison of the bio-distribution of the two viruses indicated that the expression of PB1-F2 allows a better spreading of the virus within chicken embryos. Transcriptomic profiles of lungs and blood cells were characterized at two days post-infection in chickens inoculated with the wild type (wt) or the ΔF2 mutant viruses. In lungs, the expression of PB1-F2 during the infection induced pathways related to calcium signaling and repressed a large panel of immunological functions. In blood cells, PB1-F2 was associated to a gene signature specific for mitochondrial dysfunction and down-modulated leucocytes activation. Finally we compared the effect of PB1-F2 in lungs of chickens and mice. We identified that gene signature associated to tissue damages is a PB1-F2 feature shared by the two species; by contrast, the early inhibition of immune response mediated by PB1-F2 observed in chickens is not seen in mice. In summary, our data suggest that PB1-F2 expression deeply affect the immune host response in chickens in a way that may attenuate pathogenicity, a feature differing from what was previously observed in mammal species.
2014-09-01 | GSE56506 | GEO
Project description:Mycobacterium tuberculosis persists in the lungs of mammalian hosts despite inducing an immune response dominated by the macrophage-activating cytokine interferon-gamma (IFN-gamma). We identified the M. tuberculosis phosphate uptake system component PstA1 as a factor required to resist IFN-gamma dependent immunity. A ∆pstA1 mutant was fully virulent in IFN-gamma-/- mice but was attenuated in mice lacking the IFN-gamma-inducible nitric oxide synthase (NOS2). This phenotype suggests that ∆pstA1 bacteria are hypersensitive to an IFN-gamma-dependent immune mechanism(s) other than NOS2. In other species, the Pst system participates in phosphate-responsive gene regulation by interacting with a two-component signal transduction system. We identified genes that exhibited dysregulated expression in the ∆pstA1 mutant and showed that aberrant gene expression was dependent on the two-component system response regulator RegX3. Deletion of regX3 suppressed the replication and virulence defects of ∆pstA1 bacteria in NOS2-/- mice, suggesting that the ∆pstA1 mutant is attenuated, in part, due to aberrant RegX3-dependent gene expression. Our data imply that phosphate is an important signal controlling M. tuberculosis gene expression during replication in the lung. Aerobically growing logarithmic phase Wt or pstA1/regX3/pstA1regX3 mutant strains were grown in phosphate replete media and analyzed after several hours. Experiments were repeated in triplicate (pstA1 mutant) or quadruplicate (regX3/pstA1regX3 mutant).
2013-01-01 | E-GEOD-36998 | biostudies-arrayexpress
Project description:C3heB/FeJ mice were infected with M. tuberculosis to form necrotic granulomatous lesions. FFPE samples of infected lungs with granulomas were microdissected into three distinct regions, Caseum, foamy macrophage, and Cell. Proteins were extracted from microdissected samples, followed by LC-MS/MS.
2022-09-06 | PXD030088 | JPOST Repository
Project description:CDC1551 induced more vigorous immune response in murine bone marrow derived macrophage (BMM). In contrast, in HN878-infected cells, host transcriptional response was delayed but lasted longer. HN878 induced more genes involved in host lipid metabolism than CDC1551 did. Murine bone marrow derived macrophages were infected with M. tuberculosis CDC1551 or HN878 up to 24 h. Total RNA was processed for microarray and global gene expression was read.
2011-08-29 | E-GEOD-31734 | biostudies-arrayexpress
Project description:Analysis of Mtb infected murine macrophages derived from C57Bl/6 WT, TPL2KO, IFNARKO & TPL2IFNAR DKO mice [Set 1] Tuberculosis, caused by Mycobacterium tuberculosis (Mtb), remains a leading cause of mortality and morbidity worldwide, causing approximately 1.4 million deaths per year. Key immune components for host protection during tuberculosis include the cytokines IL?12, IL?1 and TNF??, as well as IFN?? and CD4+ Th1 cells. However, immune factors determining whether individuals control infection or progress to active tuberculosis are incompletely understood. Excess amounts of type I interferon have been linked to exacerbated disease during tuberculosis in mouse models and to active disease in patients, suggesting tight regulation of this family of cytokines is critical to host resistance. In addition, the immunosuppressive cytokine IL?10 is known to inhibit the immune response to Mtb in murine models through the negative regulation of key pro-inflammatory cytokines and the subsequent Th1 response. We show here, using a combination of transcriptomic analysis, genetics and pharmacological inhibitors that the TPL-2-ERK1/2 signaling pathway is important in mediating host resistance to tuberculosis through negative regulation of type I interferon production. The TPL-2-ERK1/2 signalling pathway regulated production by macrophages of several cytokines important in the immune response to Mtb as well as regulating induction of a large number of additional genes, many in a type I IFN dependent manner. In the absence of TPL-2 in vivo, excess type I interferon promoted IL-10 production and exacerbated disease. These findings describe an important regulatory mechanism for controlling tuberculosis and reveal mechanisms by which type I interferon may promote susceptibility to this important disease. Macrophages were derived from C57Bl/6 bone marrow, plated and infected with Mtb H37Rv (or not) in duplicate wells. Samples were then harvested for RNA at time 0 (uninfected only), 15m, 30m, 1hr, 3hr, 6hr and 24hr.
2013-09-05 | E-GEOD-47672 | biostudies-arrayexpress