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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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			Action	DRS
	SRR13421056_1.fastq.gz	Fastqsanger.gz
	SRR13421056_2.fastq.gz	Fastqsanger.gz
	SRR13421057_1.fastq.gz	Fastqsanger.gz
	SRR13421057_2.fastq.gz	Fastqsanger.gz
	SRR13421058_1.fastq.gz	Fastqsanger.gz

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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. Because tissue interstitial fluid can become acidic during the septic response, we tested the hypothesis that low extracellular pH (pHe) can induce reversible metabolic and functional changes in peritoneal macrophages from C57BL/6J mice. 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 an M2-like state, with altered immune responses to LPS and slightly decreased phagocytic ability, yet they regained basal energy production, normal mitochondrial function, and proinflammatory responsiveness when neutral pHe was restored. Low pHe induces changes that support macrophage survival while rendering the cells less proinflammatory (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.

| S-EPMC8655318 | biostudies-literature

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

Acidity perturbs IL-2 responsiveness, mTORC1 and c-Myc in CD8+ T cells

Project description:CD8+T cells play a critical role in tumor control but a range of barriers in the microenvironment including low pH can suppress their function.Here, we demonstrate that acidity dampens T-cell expansion mainly due to impaired IL-2 responsiveness, blunts cytokine secretion upon re-activation, and lowers the cytolytic capacity ofCD8+T cells expressing weak affinity TCR. We further reveal decreases in both mTORC1 signaling and c-Myc levels at low pH.Mechanistically, concomitantly to nuclear/cytoplasmic acidification, mTORC1 was disrupted in a Rheb-, Akt/TSC2/PRAS40-, GATOR1- and Lkb1/AMPK -independent manner, and c-Myc levels dropped due to both decreased transcription and higher proteasome-mediated degradation. In addition, lower intracellular levels of glutamine/glutamate/aspartate and elevated proline were observed with no apparent impact on mTORC1 or c-Myc. Overall, we conclude that, due to the broad disruption caused by acidity, multiple interventions will be required to restore T-cell function unless intracellular pH can be effectively restored.

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Acidity perturbs IL-2 responsiveness, mTORC1 and c-Myc in CD8+ T cells

Project description:Acidity perturbs IL-2 responsiveness, mTORC1 and c-Myc in CD8+ T cells

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C1q reprograms innate immune memory [RNA-seq]

Project description:C1q reprograms innate immune memory [RNA-seq]

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C1q reprograms innate immune memory [ChIP-seq]

Project description:C1q reprograms innate immune memory [ChIP-seq]

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Galectin-7 reprograms skin carcinogenesis by fostering innate immune evasive programs

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Acidity-mediated induction of FoxP3+ regulatory T cells

Project description:Regulatory T cells (Tregs) are known to maintain survival and suppressive function in the presence of high levels of extracellular lactic acid. However, the effect of lactic acid on Treg induction is not known. We therfore evaluated the effect of lactic acid on Treg induction and observed an increased induction of Tregs in the presence of lactic acid. This increase occurred in a glycolysis-independent, acidity-dependent manner.

2023-03-23 | GSE217536 | GEO

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