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Transcriptional profiling of M. tuberculosis CDC1551 wild type vs aprABC null, aprBC null, aprC null and phoP transposon mutants.

ABSTRACT: Following phagocytosis by macrophages, Mycobacterium tuberculosis (Mtb) senses the intracellular environment and remodels its gene expression for growth in the phagosome. Abramovitch et.al. in this current study identified an Acid and Phagosome Regulated (aprABC) locus that is unique to the Mtb complex and whose gene expression is induced during growth in acidic environments in vitro and in macrophages. The authors propose a model where phoP senses the acidic pH of the phagosome and induces aprABC expression to fine-tune processes unique for intracellular adaptation of Mtb complex bacteria.

ORGANISM(S): Mycobacterium tuberculosis

PROVIDER: GSE22854 | GEO | 2011/07/09

SECONDARY ACCESSION(S): PRJNA128063

REPOSITORIES: GEO

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Transcriptional profiling of M. tuberculosis CDC1551 wild type vs aprABC null, aprBC null, aprC null and phoP transposon mutants.

Project description:Following phagocytosis by macrophages, Mycobacterium tuberculosis (Mtb) senses the intracellular environment and remodels its gene expression for growth in the phagosome. Abramovitch et.al. in this current study identified an Acid and Phagosome Regulated (aprABC) locus that is unique to the Mtb complex and whose gene expression is induced during growth in acidic environments in vitro and in macrophages. The authors propose a model where phoP senses the acidic pH of the phagosome and induces aprABC expression to fine-tune processes unique for intracellular adaptation of Mtb complex bacteria. This study uses microarray analyses to compare transcriptional responses of wild type Mycobacterium tuberculosis (CDC1551) to aprABC locus deletion mutants and the phoP transposon mutant. The bacteria were grown to early log phase in vented T-75 standing flasks containing 12 mL of pH 7.0 7H9 OADC medium. Transcript levels of the wild type bacteria were compared to the following mutants: aprABC null, aprBC null, aprC null, phoP::Tn mutant.

2011-07-09 | E-GEOD-22854 | biostudies-arrayexpress

Infection of bone marrow derived macrophages with M. tuberculosis CDC1551

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2012-07-11 | E-GEOD-35362 | biostudies-arrayexpress

Infection of bone marrow derived macrophages with M. tuberculosis CDC1551

2012-07-12 | GSE35362 | GEO

Gupta2019 - Restoration of cytosolic calcium inhibits Mycobacterium tuberculosis intracellular growth

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2019-11-13 | MODEL1911120004 | BioModels

Inactivated M. tuberculosis and M.tuberculosis Infection remodels the macrophage response

Project description:Background: Tuberculosis (TB) remains a major public health problem, especially in developing countries, with 1.5 million deaths annually worldwide. Macrophages (Mφs) are central to TB pathogenesis. Mφs play a key role in the outcome of the infection. More importantly, Mφs are the primary cell target of MTB, which has developed different strategies to multiply inside the Mφ phagosome. Here we aim to compare the transcriptome of Mycobacterium tuberculosis (MTB)-infected Mφs with that of cells stimulated with heat-killed MTB. Results: Here, we used live and heat-inactivated MTB to examine the impact of infection on the human macrophage response. Gene expression profiling has revealed about 3,259 genes differentially expressed in macrophages incubated with heat-inactivated MTB and 4,179 genes differentially expressed with live MTB. We found that the response to live and heat-inactivated MTB was strongly correlated (r>0.78). Conclusions: Our results show that macrophages respond in a similar manner to live and heat-inactivated MTB. We also identified some genes differentially expressed only in one condition.

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The global transcriptional profile of Mycobacterium tuberculosis during human macrophages infection

Project description:During lung infection Mycobacterium tuberculosis (Mtb) resides in macrophages and subverts the bactericidal mechanisms of these professional phagocytes. In this work we have analyzed by DNA microarray technique the global transcription profile of Mtb infecting primary human macrophages in order to identify putative bacterial pathogenic factors that can be relevant for the intracellular survival of Mtb. Keywords: time course We compared the global gene expression of the H37Rv strain of Mtb after 4 hours and 24 hours of infection of human macrophage-like THP-1 cells with the gene expression profile of the strain growing exponentially in broth cultures.

2010-05-27 | E-GEOD-6209 | biostudies-arrayexpress

The global transcriptional profile of Mycobacterium tuberculosis during human macrophages infection

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Immunopeptidomics reveals determinants of Mycobacterium tuberculosis antigen presentation on MHC class I (SureQuant data)

Project description:CD8+ T cells contribute to protective immunity to Mycobacterium tuberculosis (Mtb), but the principles that govern presentation of Mtb peptides on MHC class I (MHC-I) on the surface of infected macrophages for CD8+ T cell recognition are incompletely understood. Here, we use internal standard parallel reaction monitoring (IS-PRM, also known as SureQuant) to rigorously validate identifications of Mtb-derived MHC-I peptides obtained in data-dependent MS analyses. We further use SureQuant to quantify presentation of Mtb peptides derived from the secreted effector proteins EsxA and EsxJ across multiple experimental conditions. We show that presentation of both EsxA- and EsxJ-derived peptides requires the activity of the mycobacterial ESX-1 type VII secretion system, possibly indicating that ESX-1-mediated phagosome membrane damage allows Mtb proteins to access MHC-I antigen processing pathways. We show that this requirement is independent of type I interferon signaling that occurs downstream of phagosome damage. Treatment with inhibitors of conventional proteolytic pathways involved in MHC-I antigen processing inhibits presentation of self peptides as expected, but does not inhibit presentation of Mtb peptides, implying an alternative or redundant mechanism of processing.

2023-04-24 | PXD037843 | Pride

The sigma factor E of Mycobacterium tuberculosis modulates the inflammatory response of human THP1 cells

Project description:Mycobacterium tuberculosis (Mtb) is well adapted to survive in macrophages and usually subverts the bactericidal mechanisms of these professional phagocytes. The adaptation of Mtb to the intracellular life depends on its ability to regulate the expression of its genes. Among the most important bacterial transcription activators are the sigma factors that bind to the RNA polymerase and give it promotor specificity. Sigma factor E (SigE) controls the expression of genes that are essential for Mtb virulence. Analysis of the macrophage transcriptional response indicated that proteins encoded by the sigE regulon are involved in the modulation of the macrophage inflammatory response. We compared the global gene expression of THP1 macrophages infected with H37Rv and SigE to the gene expression profile of uninfected macrophages.

2010-05-25 | E-GEOD-7870 | biostudies-arrayexpress

A novel phenotypic drug screen identifies potent inhibitors of mycobacterial virulence protein secretion

Project description:Mycobacterium tuberculosis (Mtb) depends on protein secretion systems for intracellular survival and virulence. The major virulence determinant and ESX-1 dependent effector protein EsxA causes tissue damage and necrosis which promotes spread and dissemination of the bacterium. We developed a fibroblast survival assay (FSA) that exploits this phenotype by selecting for molecules that protect host cells from Mtb-induced lysis. Hit compounds identified in this high-throughput screen blocked the secretion of EsxA thus promoting phagosome maturation which led to substantially reduced bacterial burden in activated macrophages. Target identification studies performed on these drugs led to discovery of a benzothiophene containing histidine kinase inhibitor and a benzyloxybenzylidine hydrazine compound affecting mycobacterial metal ion homeostasis which enabled us to reveal zinc stress as a signal for EsxA secretion. Collectively, this novel drug screening approach can help to tackle the mounting problem of antibiotic-resistant mycobacteria by largely extending the target spectrum of small molecule libraries.

2015-05-15 | GSE58314 | GEO

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