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Extracellular acidity reprograms macrophage metabolism and innate responsiveness

ABSTRACT: Extracellular acidity reprograms macrophage metabolism and innate responsiveness

PROVIDER: PRJNA691584 | ENA |

REPOSITORIES: ENA

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Extracellular acidity reprograms macrophage metabolism and innate responsiveness

Project description:Although organ hypofunction and immunosuppression are life-threatening features of severe sepsis, the hypofunctioning organs and immune cells usually regain normal functionality if patients survive. We tested the hypothesis that low extracellular pH (pHe) can induce reversible metabolic and functional changes in tissue macrophages. When compared with macrophages cultured at normal pHe, macrophages living in an acidic medium used less glucose and exogenous fatty acid to produce ATP. Lactate, glutamine, and de novo synthesized fatty acids supported ATP production by mitochondria that gained greater mass, maximal oxygen consumption rate, and spare respiratory capacity. The cells transitioned to a M2-like state, with altered immune responses to LPS and slightly decreased phagocytic ability, yet they regained basal energy production, normal mitochondrial function and pro-inflammatory responsiveness when neutral pHe was restored. Low pHe induces changes that support macrophage survival while rendering the cells less pro-inflammatory (more ‘tolerant’) and less able to phagocytose bacteria. Macrophage responses to low interstitial pH may contribute to the reversible organ hypofunction and immunoparalysis noted in many patients with sepsis.

2021-04-15 | GSE164697 | GEO

MITF reprograms the extracellular matrix and focal adhesion in melanoma

Project description:MITF reprograms the extracellular matrix and focal adhesion in melanoma

| PRJNA686997 | ENA

The lung environment controls alveolar macrophage metabolism and responsiveness during type-2 inflammation.

Project description:Fine control of macrophage activation is required to prevent inflammatory disease, particularly at barrier sites such as the lung. However, the dominant mechanisms that regulate pulmonary MΦs during inflammation are currently poorly understood. Here we show that airway MΦs are substantially less able to respond to the canonical type-2 cytokine IL-4, which underpins allergic disease and parasite worm infections, than lung tissue or peritoneal cavity MΦs. We reveal that MΦ hypo-responsiveness to IL-4 is dictated by the lung environment, though independent of the host microbiota or the prominent lung extracellular matrix components surfactant protein D and mucin 5b. Rather, compared to cavity MΦs, airway MΦs display severely dysregulated metabolism. Strikingly, upon removal from the lung, alveolar MΦs regain IL-4 responsiveness in a process dependent upon glycolysis. Thus, we propose that impaired glycolysis within the pulmonary niche is a central determinant for regulation of MΦ responsiveness during type-2 inflammation.

2019-03-26 | GSE126309 | GEO

SMALL EXTRACELLULAR VESICLE REGULATION OF MITOCHONDRIAL DYNAMICS REPROGRAMS A HYPOXIC TUMOR MICROENVIRONMENT

Project description:SMALL EXTRACELLULAR VESICLE REGULATION OF MITOCHONDRIAL DYNAMICS REPROGRAMS A HYPOXIC TUMOR MICROENVIRONMENT

| PRJNA645917 | ENA

Maternal slimming reprograms metabolic gene expression in mice offspring

Project description:This SuperSeries is composed of the following subset Series: GSE40471: Maternal slimming reprograms metabolic gene expression in mice offspring (NimbleGen expression) GSE40477: Maternal slimming reprograms metabolic gene expression in mice offspring (NimbleGen methylation) GSE40478: Maternal slimming reprograms metabolic gene expression in mice offspring (mRNA-Seq) Refer to individual Series

2012-08-30 | E-GEOD-40479 | biostudies-arrayexpress

Mitohormesis reprograms macrophage metabolism to enforce tolerance.

Project description:Mitohormesis reprograms macrophage metabolism to enforce tolerance.

| PRJNA717764 | ENA

Innate immune stimulation of whole blood reveals IFN-1 hyper-responsiveness in type 1 diabetes

Project description:Innate immune stimulation of whole blood reveals IFN-1 hyper-responsiveness in type 1 diabetes

| PRJNA610180 | ENA

Mitohormesis reprograms macrophage metabolism to enforce tolerance [BMDM_ChIPseq]

Project description:Mitohormesis reprograms macrophage metabolism to enforce tolerance [BMDM_ChIPseq]

| PRJNA717767 | ENA

Mitohormesis reprograms macrophage metabolism to enforce tolerance [vWAT_mac_RNAseq]

Project description:Mitohormesis reprograms macrophage metabolism to enforce tolerance [vWAT_mac_RNAseq]

| PRJNA717768 | ENA

Mitohormesis reprograms macrophage metabolism to enforce tolerance [BMDM_OHestrogen_RNAseq]

Project description:Mitohormesis reprograms macrophage metabolism to enforce tolerance [BMDM_OHestrogen_RNAseq]

| PRJNA717769 | ENA

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