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Mus musculus

ABSTRACT: Immune-Responsive Gene 1 expression in myeloid cells prevents neutrophil mediated immunopathology during Mycobacterium tuberculosis infection, in vitro neutrophils data

PROVIDER: PRJNA385148 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5495120.fastq.gz	Fastqsanger.gz
	SRR5495111.fastq.gz	Fastqsanger.gz
	SRR5495121.fastq.gz	Fastqsanger.gz
	SRR5495112.fastq.gz	Fastqsanger.gz
	SRR5495122.fastq.gz	Fastqsanger.gz

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Immune-Responsive Gene 1 expression in myeloid cells prevents neutrophil mediated immunopathology during Mycobacterium tuberculosis infection.

Project description:Immune-Responsive Gene 1 expression in myeloid cells prevents neutrophil mediated immunopathology during Mycobacterium tuberculosis infection.

| PRJNA385136 | ENA

Immune-Responsive Gene 1 expression in myeloid cells prevents neutrophil mediated immunopathology during Mycobacterium tuberculosis infection [macrophage]

Project description:Immune-Responsive Gene 1 expression in myeloid cells prevents neutrophil mediated immunopathology during Mycobacterium tuberculosis infection [macrophage]

| PRJNA422778 | ENA

Mus musculus

Project description:Immune-Responsive Gene 1 expression in myeloid cells prevents neutrophil mediated immunopathology during Mycobacterium tuberculosis infection, in vivo neutrophil data

| PRJNA385147 | ENA

Immune-Responsive Gene 1 expression in myeloid cells prevents neutrophil mediated immunopathology during Mycobacterium tuberculosis infection [macrophage]

Project description:Immune-Responsive Gene 1 (Irg1) is a mitochondrial enzyme that produces itaconate under inflammatory conditions principally in cells of myeloid lineage. Cell culture studies suggest that itaconate regulates inflammation through inhibitory effects on cytokine and reactive oxygen species production. To evaluate the functions of Irg1 in vivo, we challenged wild-type (WT) and Irg1-/- mice with Mycobacterium tuberculosis (Mtb) and monitored disease progression. Irg1-/- but not WT mice succumbed rapidly to Mtb, and mortality was associated with increased infection, inflammation, and pathology. Infection of LysM-Cre Irg1fl/fl, MPR8-Cre Irg1fl/fl, and CD11c-Cre Irg1fl/fl conditional knockout mice along with neutrophil depletion experiments revealed a role for Irg1 in alveolar macrophages and LysM+ myeloid cells in preventing neutrophil-mediated immunopathology and disease. RNA-seq analyses suggest that Irg1 and its production of itaconate temper Mtb-induced inflammatory responses in myeloid cells at the transcriptional level. Thus, Irg1 modulates inflammation to curtail Mtb-induced lung disease.

2018-02-15 | GSE108188 | GEO

Immune-Responsive Gene 1 expression in myeloid cells prevents neutrophil mediated immunopathology during Mycobacterium tuberculosis infection, in vitro neutrophils data

Project description:Immune-Responsive Gene 1 (Irg1) is a mitochondrial enzyme that produces itaconate under inflammatory conditions principally in cells of myeloid lineage. Cell culture studies suggest that itaconate regulates inflammation through inhibitory effects on cytokine and reactive oxygen species production. To evaluate the functions of Irg1 in vivo, we challenged wild-type (WT) and Irg1 KO mice with Mycobacterium tuberculosis (Mtb) and monitored disease progression. Irg1 KO but not WT mice succumbed rapidly to Mtb, and mortality was associated with increased infection, inflammation, and pathology. Infection of LysM-Cre Irg1 flox, MPR8-Cre Irg1 flox, and CD11c-Cre Irg1 flox conditional knockout mice along with neutrophil depletion experiments revealed a role for Irg1 in alveolar macrophages and LysM+ myeloid cells in preventing neutrophil-mediated immunopathology and disease. RNA-seq analyses suggest that Irg1 and its production of itaconate temper Mtb-induced inflammatory responses in myeloid cells at the transcriptional level. Thus, Irg1 modulates inflammation to curtail Mtb-induced lung disease.

2017-08-30 | GSE98456 | GEO

Immune-Responsive Gene 1 expression in myeloid cells prevents neutrophil mediated immunopathology during Mycobacterium tuberculosis infection, in vivo neutrophil data

Project description:Immune-Responsive Gene 1 (Irg1) is a mitochondrial enzyme that produces itaconate under inflammatory conditions principally in cells of myeloid lineage. Cell culture studies suggest that itaconate regulates inflammation through inhibitory effects on cytokine and reactive oxygen species production. To evaluate the functions of Irg1 in vivo, we challenged wild-type (WT) and Irg1 KO mice with Mycobacterium tuberculosis (Mtb) and monitored disease progression. Irg1 KO but not WT mice succumbed rapidly to Mtb, and mortality was associated with increased infection, inflammation, and pathology. Infection of LysM-Cre Irg1 flox, MPR8-Cre Irg1 flox, and CD11c-Cre Irg1 flox conditional knockout mice along with neutrophil depletion experiments revealed a role for Irg1 in alveolar macrophages and LysM+ myeloid cells in preventing neutrophil-mediated immunopathology and disease. RNA-seq analyses suggest that Irg1 and its production of itaconate temper Mtb-induced inflammatory responses in myeloid cells at the transcriptional level. Thus, Irg1 modulates inflammation to curtail Mtb-induced lung disease.

2017-08-30 | GSE98457 | GEO

Transcriptome analysis of lung neutrophils from mice infected with Mycobacterium tuberculosis

Project description:Neutrophils are accumulated in mouse lungs following Mycobacterium tuberculosis infections. Increased influx of neutrophils is associated with increased susceptibility to disease, but the underlying mechanisms of neutrophil mediated Tuberculosis disease pathogenesis is poorly understood. To understand the transcriptomic differences between resistant (C57 BL/6) and susceptible (C3HeB/FeJ) mouse lung neutrophils, we sorted them at Day 29 post infection and analyzed them by bulk mRNA sequencing.

2024-09-27 | GSE244230 | GEO

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

Characterization of myeloid cells in acute and chronic LCMV infection by scRNA-seq

Project description:The immune response to a chronic viral infection is uniquely tailored to balance viral control and immunopathology. The role of myeloid cells in shaping the response to chronic viral infection, however, is poorly understood. Single-cell RNA sequencing of myeloid cells during acute and chronic LCMV infection was performed to address this question. We discovered a cluster of suppressive neutrophils that is enriched in chronic versus acute infection. Furthermore, suppressive neutrophils highly expressed the gene encoding PIM1, a kinase known to promote mitochondrial fitness and cell survival. Pharmacological inhibition of PIM1 selectively diminished suppressive neutrophil-mediated immunosuppression without affecting the function of monocytic myeloid derived suppressor cells (M-MDSCs). Decreased accumulation of suppressive neutrophils led to increased CD8 T cell function and viral control. Mechanistically, PIM kinase activity was required for maintaining fused mitochondrial networks in suppressive neutrophils, but not in M-MDSCs, and loss of PIM kinase function caused increased apoptosis of suppressive neutrophils.

2021-05-05 | GSE167204 | GEO

Transcriptomic analysis reveals inflammasome-dependent mechanism for early neutrophil response to Mycobacterium Marinum

Project description:The mechanisms that govern the neutrophil response to Mycobacterium tuberculosis remain poorly understood. In this study we utilize an innovative binary approach in zebrafish to perform in depth profiling of the initial response of neutrophils to Mycobacterium marinum, by in vivo biotinylation of neutrophil nuclei and subsequent rapid isolation directly from the in vivo context. RNA-seq and differential expression analysis of the neutrophil nuclear transcriptome reveals a significant upregulation in both damage-sensing and effector components of the inflammasome, including caspase b, wu:fb15h11 (NLRC3 ortholog) and il1β. Crispr/Cas9-mediated knockdown of caspase b, which mediates its effects by the proteolytic processing of il1β, results in increased bacterial burden and less infiltration of macrophages to sites of mycobacterium infection, thus impairing granuloma development. We also show that a number of immediate early response genes (IEGs) are responsible for orchestrating the initial response to mycobacterial infection in neutrophils. Further perturbation of the IEGs revealed egr3 as a key transcription factor regulating il1β transcription.

2017-08-31 | GSE92740 | GEO

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