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Neutrophils-derived itaconate facilitates viral infection via alkylating GDI2 II

ABSTRACT: The objective was to investigate the disparity in gene expression between IRG1+/+ BMDMs and IRG1-/- BMDMs following VSV infection.

ORGANISM(S): Mus musculus

PROVIDER: GSE249683 | GEO | 2024/06/01

REPOSITORIES: GEO

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Neutrophils-derived itaconate facilitates viral infection via alkylating GDI2 [RNA-seq]

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Neutrophils-derived itaconate facilitates viral infection via alkylating GDI2 [scRNA-seq]

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Neutrophils-derived itaconate facilitates viral infection via alkylating GDI2

Project description:This SuperSeries is composed of the SubSeries listed below.

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

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Neutrophils-derived itaconate facilitates viral infection via alkylating GDI2

Project description:Neutrophils-derived itaconate facilitates viral infection via alkylating GDI2

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Neutrophils-derived itaconate facilitates viral infection via alkylating GDI2 II

Project description:Neutrophils-derived itaconate facilitates viral infection via alkylating GDI2 II

| PRJNA1050190 | ENA

Neutrophils-derived itaconate facilitates viral infection via alkylating GDI2 [RNA-seq]

Project description:Neutrophils-derived itaconate facilitates viral infection via alkylating GDI2 [RNA-seq]

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Neutrophils-derived itaconate facilitates viral infection via alkylating GDI2 [scRNA-seq]

Project description:Neutrophils-derived itaconate facilitates viral infection via alkylating GDI2 [scRNA-seq]

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Comparative evaluation of metabolic, electrophilic, and immunologic effects of itaconate and its ester derivatives on macrophage activation

Project description:Itaconate is a metabolite naturally produced in large amounts in macrophages after exposure to immune stimulation. Following the discovery of itaconate’s immunoregulatory properties, several ester derivatives of this dicarboxylic acid were designed to further examine its role. We evaluated the metabolic, electrophilic, and immunologic profiles of macrophages treated with unmodified itaconate and a panel of itaconate derivatives. We found that only unmodified itaconate strongly enhances LPS-induced IFNb secretion after 12h pre-treatment. Thus, we compared the transcriptional profile of wild type and Irg1-/- cells, which are unable to produce itaconate, after 24h LPS stimulation. We find that cells lacking itaconate have impaired downstream type I interferon signaling, and that addition of itaconate Irg1-/- BMDMs restores this signaling back to levels comparable to wild type. This data highlights the role of itaconate as an immunoregulatory metabolite, and highlights the importance of using unmodified itaconate or genetic knockout models in future mechanistic studies.

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