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IRG1 Promotes Neutrophil Reverse Migration and Alleviates Local Inflammation

ABSTRACT: IRG1 Promotes Neutrophil Reverse Migration and Alleviates Local Inflammation

PROVIDER: PRJNA1100455 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28681749.fastq.gz	Fastqsanger.gz
	SRR28681750.fastq.gz	Fastqsanger.gz
	SRR28681751.fastq.gz	Fastqsanger.gz
	SRR28681752.fastq.gz	Fastqsanger.gz
	SRR28681753.fastq.gz	Fastqsanger.gz

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IRG1 Promotes Neutrophil Reverse Migration and Alleviates Local Inflammation

Project description:Polymorphonuclear neutrophil (PMN) infiltration at inflammatory site plays a critical role in inflammation. PMN reverse migration (rM) describes the phenomenon that PMNs migrate away from inflammatory site back into the vasculature, and its role within inflammatory scenarios remains to be fully determined. This study aimed to investigate the mechanism underlying PMN rM and its role in inflammation. First, we demonstrated PMN rM in a mouse model of LPS-induced acute lung inflammation. By single-cell RNA sequencing (scRNA-seq), we demonstrated that reverse migrated (rM-ed) PMNs in blood expressed high level of immuneresponsive gene 1 (Irg1), the encoding gene of cis-aconitate decarboxylase (ACOD1).

2025-04-14 | GSE263953 | 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.

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Transcriptome profiling of irg1 mutant leaf of Medicago truncatula

Project description:To gain a molecular understanding of the loss-of-function mutation of a transcription factor involved in leaf morphogenesis impacts symmetric cuticular wax loading in M. truncatula, we compared the transcript profiles of wild-type R108 and three independent irg1/palm1 homozygous null mutant lines (irg1-1, irg1-2, and irg1-5).

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

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Targeting IRG1 in tumor-associated macrophages for cancer therapy

Project description:Immune-responsive gene 1 (IRG1) is a mitochondrial aconitate decarboxylase and can produce the immunomodulatory metabolite itaconic acid (ITA). However, its role in modulating the function of tumor-associated macrophages (TAMs) remains elusive. Here, we show that IRG1 is expressed in TAMs in human tumors and mouse models of cancer. Tumor cells induce Irg1 expression in macrophages which dampens the inflammatory response and restricts M1-like TAM polarization. In contrast, Irg1-deficent macrophages acquire more proinflammatory M1-like features, promote immunogenic antigen presentation, and enhance cytotoxic T cell infiltration into tumor sites. Consequently, Irg1 deficiency suppresses the growth of mouse syngeneic tumors, including melanoma, colorectal cancer, breast cancer, and pancreatic cancer. Irg1-deficient macrophages not only dictate the tumoricidal effect but enhance the efficacy of anti-PD(L)1 immunotherapy. In conclusion, our data identify IRG1 as a myeloid immune check point gene and foster the development of genetic or pharmacologic targeting of IRG1 for skewing macrophages toward an anti-tumor phenotype to treat a broad spectrum of cancer.

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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.

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Staphylococcus aureus stimulates neutrophil itaconate production that suppresses the oxidative burst

Project description:Neutrophils are critical in the host defense against Staphylococcus aureus, a major human pathogen. However, even in the setting of a robust neutrophil response, S. aureus can cause persistent infection. Here we demonstrate that S. aureus impairs neutrophil function by triggering the production of the anti-inflammatory metabolite, itaconate. The enzyme that synthesizes itaconate, Irg1, is selectively expressed in neutrophils during S. aureus pneumonia. Itaconate inhibits neutrophil glycolysis and oxidative burst, which impairs survival and bacterial killing. In a murine pneumonia model, neutrophil Irg1 expression protects critical lung cell populations from oxidative stress but compromises bacterial clearance. S. aureus is thus able to evade innate immune clearance by targeting neutrophil metabolism and inducing the production of the antiinflammatory metabolite itaconate.

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Lactiplantibacillus plantarum strain:IRG1

Project description:Lactobacillus plantarum IRG1 Genome sequencing and assembly

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Effects of Irg1-itaconate or Hemin on gene expression in macrophages [RNA-seq]

Project description:To investigate the role of Irg1-itaconate or Hemin in macrophages, bone marrow-derived macrophages (BMDMs) from WT mice and Irg1 KO mice were extracted and cultured. After 7 days of cells culture, the BMDMs from WT mice were treated 120 μM 4-octyl itaconate (4-OI) for 15 h, 15 μM Hemin for 12 h, and the BMDMs from Irg1 KO mice and WT mice were treated Vehicle for 12 h. We then performed gene expression profiling analysis using data obtained from RNA-seq of 4-OI, Hemin or vehicle treated WT BMDMs and Irg1 KO BMDMs.

2024-06-28 | GSE221734 | GEO

miRNA overexpression modulates neutrophil migration

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