期刊
CELL METABOLISM
卷 27, 期 5, 页码 988-+出版社
CELL PRESS
DOI: 10.1016/j.cmet.2018.03.019
关键词
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资金
- Monash MicroImaging Facility
- Australian National Health and Medical Research Council (NHMRC) [APP1081072, APP1101562]
- Australian Research Council Fellowships [DE140101164, FT170100313]
- Australian Research Council [FT170100313] Funding Source: Australian Research Council
To fight infections, macrophages undergo a metabolic shift whereby increased glycolysis fuels antimicrobial inflammation and killing of pathogens. Here we demonstrate that the pathogen Candida albicans turns this metabolic reprogramming into an Achilles' heel for macrophages. During Candida-macrophage interactions intertwined metabolic shifts occur, with concomitant upregulation of glycolysis in both host and pathogen setting up glucose competition. Candida thrives on multiple carbon sources, but infected macrophages are metabolically trapped in glycolysis and depend on glucose for viability: Candida exploits this limitation by depleting glucose, triggering rapid macrophage death. Using pharmacological or genetic means to modulate glucose metabolism of host and/or pathogen, we show that Candida infection perturbs host glucose homeostasis in the murine candidemia model and demonstrate that glucose supplementation improves host outcomes. Our results support the importance of maintaining glucose homeostasis for immune cell survival during Candida challenge and for host survival in systemic infection.
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