Infection and Immunity Program and the Department of Biochemistry & Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, Vic., Australia.
EMBO Rep. 2019 Jul;20(7):e47995. doi: 10.15252/embr.201947995. Epub 2019 Jun 21.
Antimicrobial drug resistance is threatening to take us to the "pre-antibiotic era", where people are dying from preventable and treatable diseases and the risk of hospital-associated infections compromises the success of surgery and cancer treatments. Development of new antibiotics is slow, and alternative approaches to control infections have emerged based on insights into metabolic pathways in host-microbe interactions. Central carbon metabolism of immune cells is pivotal in mounting an effective response to invading pathogens, not only to meet energy requirements, but to directly activate antimicrobial responses. Microbes are not passive players here-they remodel their metabolism to survive and grow in host environments. Sometimes, microbes might even benefit from the metabolic reprogramming of immune cells, and pathogens such as Candida albicans, Salmonella Typhimurium and Staphylococcus aureus can compete with activated host cells for sugars that are needed for essential metabolic pathways linked to inflammatory processes. Here, we discuss how metabolic interactions between innate immune cells and microbes determine their survival during infection, and ways in which metabolism could be manipulated as a therapeutic strategy.
抗菌药物耐药性正威胁着将我们带回到“抗生素前时代”，人们会死于可预防和可治疗的疾病，医院相关感染的风险会危及手术和癌症治疗的成功。新型抗生素的开发进展缓慢，而基于对宿主-微生物相互作用中代谢途径的深入了解，已经出现了控制感染的替代方法。免疫细胞的中心碳代谢对于对入侵病原体产生有效反应至关重要，不仅是为了满足能量需求，还可以直接激活抗菌反应。微生物在这里并不是被动的参与者——它们会重塑代谢以在宿主环境中生存和生长。有时，微生物甚至可能受益于免疫细胞的代谢重编程，而像白色念珠菌、伤寒沙门氏菌和金黄色葡萄球菌这样的病原体可以与被激活的宿主细胞竞争对与炎症过程相关的必要代谢途径至关重要的糖。在这里，我们讨论了先天免疫细胞和微生物之间的代谢相互作用如何决定它们在感染期间的存活，以及可以将代谢作为一种治疗策略进行操纵的方式。
