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Mouse transcriptome reveals potential signatures of protection and pathogenesis in human tuberculosis [lung array]

ABSTRACT: Characterisation of blood and lung global transcriptional responses to Mycobacterium tuberculosis infection in distinct mouse models of Tuberculosis

ORGANISM(S): Mus musculus

PROVIDER: GSE140944 | GEO | 2020/01/09

REPOSITORIES: GEO

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Mouse transcriptome reveals potential signatures of protection and pathogenesis in human tuberculosis [blood array]

Project description:Characterisation of blood and lung global transcriptional responses to Mycobacterium tuberculosis infection in distinct mouse models of Tuberculosis

2020-01-09 | GSE140943 | GEO

Mouse transcriptome reveals novel signatures of protection and pathogenesis in human tuberculosis [lung]

Project description:Characterisation of blood and lung global transcriptional responses to Mycobacterium tuberculosis infection in distinct mouse models of Tuberculosis

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Project description:Characterisation of blood and lung global transcriptional responses to Mycobacterium tuberculosis infection in distinct mouse models of Tuberculosis

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Mouse transcriptome reveals potential signatures of protection and pathogenesis in human tuberculosis [lung array]

Project description:Mouse transcriptome reveals potential signatures of protection and pathogenesis in human tuberculosis [lung array]

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Mouse transcriptome reveals potential signatures of protection and pathogenesis in human tuberculosis.

Project description:Although mouse infection models have been extensively used to study the host response to Mycobacterium tuberculosis, their validity in revealing determinants of human tuberculosis (TB) resistance and disease progression has been heavily debated. Here, we show that the modular transcriptional signature in the blood of susceptible mice infected with a clinical isolate of M. tuberculosis resembles that of active human TB disease, with dominance of a type I interferon response and neutrophil activation and recruitment, together with a loss in B lymphocyte, natural killer and T cell effector responses. In addition, resistant but not susceptible strains of mice show increased lung B cell, natural killer and T cell effector responses in the lung upon infection. Notably, the blood signature of active disease shared by mice and humans is also evident in latent TB progressors before diagnosis, suggesting that these responses both predict and contribute to the pathogenesis of progressive M. tuberculosis infection.

| S-EPMC7116040 | biostudies-literature

Mouse transcriptome reveals potential signatures of protection and pathogenesis in human tuberculosis [blood array]

Project description:Mouse transcriptome reveals potential signatures of protection and pathogenesis in human tuberculosis [blood array]

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In-vivo Gene Signatures of Mycobacterium tuberculosis In C3HeB/FeJ Mice

Project description:In-vivo Gene Signatures of Mycobacterium tuberculosis In C3HeB/FeJ Mice

2015-07-11 | GSE70765 | GEO

Genome-wide analysis of gene expression in lung cells from metformin treated Mycobacterium tuberculosis infected mice

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.

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ZBTB7B (ThPOK) IS REQUIRED FOR PATHOGENESIS OF CEREBRAL MALARIA AND PROTECTION AGAINST PULMONARY TUBERCULOSIS

Project description:We used a genome-wide screen in N-ethyl-N-nitrosourea (ENU)-mutagenized mice to identify genes in which recessive loss-of-function mutations protect against pathological neuroinflammation. We identified an R367Q mutation in the ZBTB7B (ThPOK) protein in which homozygosity causes protection against experimental cerebral malaria (ECM) caused by infection with Plasmodium berghei ANKA. Zbtb7bR367Q homozygous mice show a defect in the lymphoid compartment expressed as severe reduction in the number of single-positive CD4 T cells in the thymus and in the periphery, reduced brain infiltration of proinflammatory leukocytes in P. berghei ANKA-infected mice, and reduced production of proinflammatory cytokines by primary T cells ex vivo and in vivo. Dampening of proinflammatory immune responses in Zbtb7bR367Q mice is concomitant to increased susceptibility to infection with avirulent (Mycobacterium bovis BCG) and virulent (Mycobacterium tuberculosis H37Rv) mycobacteria. The R367Q mutation maps to the first DNA-binding zinc finger domain of ThPOK and causes loss of base contact by R367 in the major groove of the DNA, which is predicted to impair DNA binding. Global immunoprecipitation of ThPOK-containing chromatin complexes coupled to DNA sequencing (ChIP-seq) identified transcriptional networks and candidate genes likely to play key roles in CD4+ CD8+ T cell development and in the expression of lineage-specific functions of these cells. This study highlights ThPOK as a global regulator of immune function in which alterations may affect normal responses to infectious and inflammatory stimuli.

2019-12-17 | GSE142069 | GEO

mRNA degradation in Mycobacterium tuberculosis

Project description:This SuperSeries is composed of the following subset Series: GSE36341: mRNA degradation in Mycobacterium tuberculosis under aerobic conditions GSE36342: mRNA degradation in Mycobacterium smegmatis under aerobic conditions GSE36343: mRNA degradation in Mycobacterium tuberculosis during cold and hypoxic stress GSE36344: mRNA degradation in Mycobacterium tuberculosis with DosR ectopically induced Refer to individual Series

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