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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. 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.

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