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Comprehensive profiling of the early lung immune responses in the mouse model of tuberculosis

ABSTRACT: The lung host immune responses following M.tuberculosis infection in the mouse model of tuberculosis were assayed by studying the gene expression profiles at day 0, day 12, 15 and 21 post infection

ORGANISM(S): Mus musculus

PROVIDER: GSE23014 | GEO | 2010/07/21

SECONDARY ACCESSION(S): PRJNA131515

REPOSITORIES: GEO

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Comprehensive profiling of the early lung immune responses in the mouse model of tuberculosis

Project description:The lung host immune responses following M.tuberculosis infection in the mouse model of tuberculosis were assayed by studying the gene expression profiles at day 0, day 12, 15 and 21 post infection Mice were infected with M.tuberculosis via the aerosol route and the host gene induction during early immune response studied

2010-07-21 | E-GEOD-23014 | biostudies-arrayexpress

RNA sequencing of neutrophils isolated from lung, spleen and bone marrow of Mycobacterium tuberculosis infected mice

Project description:Mycobacterium tuberculosis infection of mice elicits a robust neutrophil influx that associates with poor outcome from tuberculosis (TB). However, the mechanism by which neutrophils contribute to TB disease pathogenesis is not understood. To gain insights into the pathological functions of neutrophils, the current study performs bulk mRNA sequencing from the neutrophils isolated from lung, spleen and bone marrow of resistant (C57BL/6) and susceptible (IL-1R1 KO) mice at 28 days post M.tuberculosis HN878 infection.

2024-02-29 | GSE203118 | GEO

Host resistance to pulmonary infection with Mycobacterium tuberculosis is mediated by IL-1alpha.

Project description:Background: M.tuberculosis is one of the most prevalent and deadly human pathogens. The molecular mechanisms determining the outcomes of an infection with M.tuberculosis, that range from resistance to an active progressive disease, remain incompletely understood. Here we provide the evidence that IL-1alpha plays a critical and non-redundant role in enabling host resistance to pulmonary M.tuberculosis infection in mice that develop functional pathogen-specific adaptive immunity. Mechanistically, IL-1alpha-deficient mice fail to control M.tuberculosis replication in vivo at a level of individual infected cells and succumb to progressive disease at the late phase of infection. Furthermore, we show that IL-1alpha from hematopoietic compartment through IL-1RI operates upstream of TNFRI-signaling pathway and the lack of IL-1alpha leads to the continuous influx of monocytes that acquire a hyper-inflammatory phenotype and contribute to pathology, rather than to a pathogen control. Cell-type-specific restoration of IL-1alpha expression in CD11c+ subsets of lung leukocytes resulted in reduced levels of inflammatory marker expression on lung cells and improved survival IL-1alpha-deficient mice after M.tuberculosis infection. In humans, genetic analysis of single nucleotide polymorphisms in 14 genes implicated in IL-1-IL-1R signaling pathway revealed association of genetic variations in IL-1alpha and IL-1RAP genes with human susceptibility to pulmonary tuberculosis. Our results implicate IL-1alpha as a principal factor of host resistance to M.tuberculosis and IL-1alpha-driven cell-cell crosstalk as a key step in triggering M.tuberculosis control mechanisms that are critical for host survival.

2019-09-03 | GSE32619 | GEO

Transcriptional Responses of M. tuberculosis to inhibitors of metabolism

Project description:Transcriptional profiling of M.tuberculosis was performed using 430 whole-genome microarrays to measure the effects of 75 different drugs, drug combinations or different growth conditions at various times relative to a sample of logarithmically growing MTb. Analysis of this data set revealed 150 underlying clusters of coordinately regulated genes as described in Boshoff et al., 2004. Keywords = Gene clusters Keywords = Mechanism of action Keywords = tuberculosis Keywords = antimycobacterial drugs Keywords = natural product Keywords = respiration

2004-09-01 | E-GEOD-1642 | biostudies-arrayexpress

Transcriptional Responses of M. tuberculosis to inhibitors of metabolism

2004-09-01 | GSE1642 | GEO

Novel data integration approaches identify concordant and discordant immune responses between mice and humans [mouse]

Project description:We have conducted experiments to compare transcriptional response to tuberculosis (TB) in whole blood in two different TB murine models (susceptible 129S2 strain and resistant C57BL/6 strain) in time points day 1, day 7, day 14 and day 21 after infection.

2017-09-21 | GSE89389 | GEO

Transcriptional profiles of lung macrophage subsets in Mycobacterium Tuberculosis infection

Project description:We investigated transcriptional responses of different lung macrophage lineages during M.tuberculosis infection by RNAseq. Our data revealed that different lineages of macrophages respond differentially to M.Tuberculosis infection.

2018-02-21 | GSE108844 | GEO

Response of M. tuberculosis to 8 hour exposure to vitamin C

Project description:Transcriptional profiling of M.tuberculosis to 10 mM vitamin C at 8 h. This was compared to gene expression profile of untreated M. tuberculosis culture.

2014-10-01 | GSE60376 | GEO

Response of M. tuberculosis to 8 hour exposure to vitamin C

Project description:Transcriptional profiling of M.tuberculosis to 10 mM vitamin C at 8 h. This was compared to gene expression profile of untreated M. tuberculosis culture. Organism: Mycobacterium tuberculosis H37Rv, Genotypic Technology designed Custom Mycobacterium tuberculosis H37Rv Whole Genome 8x15k GE Microarray (AMADID-020181)

2014-10-01 | E-GEOD-60376 | biostudies-arrayexpress

Temporal response of Mycobacterium tuberculosis H37Rv to vitamin C exposure.

Project description:Transcriptional profiling of M.tuberculosis to 10 mM vitamin C at 0.25, 0.5, 1, 2 , 4, 8 and 24 h compared to gene expression profile of untreated M. tuberculosis culture (0 h).

2018-01-31 | GSE101048 | GEO

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