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

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

PROVIDER: PRJNA1051036 | ENA |

REPOSITORIES: ENA

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Neutrophils-derived itaconate facilitates viral infection via alkylating GDI2

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

| PRJNA1051031 | ENA

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 [scRNA-seq]

Project description: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.

2024-12-25 | GSE249857 | GEO

Neutrophils-derived itaconate facilitates viral infection via alkylating GDI2 II

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

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Itaconate-producing neutrophils regulate local and systemic inflammation following trauma

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

Project description:The purpose is to investigate alterations in gene expression across diverse cellular subsets within the pulmonary tissue of mouse infected with VSV.

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

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Itaconate-producing neutrophils regulate local and systemic inflammation following trauma

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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.

2023-01-01 | GSE215195 | GEO

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