Metabolic immunity against microbes

被引:6
|
作者
Kreimendahl, Sebastian [1 ]
Pernas, Lena [1 ,2 ,3 ,4 ]
机构
[1] Max Planck Inst Biol Ageing, Cologne, Germany
[2] Howard Hughes Med Inst, Chevy Chase, MD 20815 USA
[3] Univ Calif Angeles, Dept Microbiol Immunol & Mol Genet, Los Angeles, CA 90095 USA
[4] Univ Cologne, Cologne Excellence Cluster Cellular Stress Respons, Cologne, Germany
基金
欧洲研究理事会;
关键词
INDUCIBLE NITRIC-OXIDE; PARASITE TOXOPLASMA-GONDII; IRON HOMEOSTASIS; COLONIZATION RESISTANCE; BACTERICIDAL ACTIVITY; MURINE MACROPHAGES; HUMAN-FIBROBLASTS; ESCHERICHIA-COLI; SAMHD1; RESTRICTS; GAMMA-INTERFERON;
D O I
10.1016/j.tcb.2023.10.013
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Pathogens, including viruses, bacteria, fungi, and parasites, remodel the metabolism of their host to acquire the nutrients they need to proliferate. Thus, host cells are often perceived as mere exploitable nutrient pools during infection. Mounting reports challenge this perception and instead suggest that host cells can actively reprogram their metabolism to the detriment of the microbial invader. In this review, we present metabolic mechanisms that host cells use to defend against pathogens. We highlight the contribution of domesticated microbes to host defenses and discuss examples of host-pathogen arms races that are derived from metabolic conflict.
引用
收藏
页码:496 / 508
页数:13
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