Takeda Kazuyoshi, Okumura Ko
Laboratory of Cell Biology, Research Support Center, Graduate School of Medicine, Juntendo University.
Department of Biofunctional Micribiota, Graduate School of Medicine, Juntendo University.
Biomed Res. 2021;42(5):173-179. doi: 10.2220/biomedres.42.173.
Nicotinamide mononucleotide (NMN), a key nicotinamide adenine dinucleotide (NAD) intermediate, has been shown to ameliorate various pathologies in elderly mouse disease models. Natural killer (NK) cells are important innate immune cells; however, their functions decline with aging. In this study, we examined the effect of NMN treatment on NK cells in mice. Intraperitoneal administration of NMN augmented NK cell cytotoxic activity in both young and elderly B6 mice as well as young BALB/c mice. Oral administration of NMN also increased NK cell cytotoxicity in elderly B6 and BALB/c mice. However, the NK cell population was not increased in the mice whose NK cell cytotoxic activity was activated by NMN. Interestingly, NMN administration did not augment NK cell cytotoxic activity in IFN-γ deficient mice. These results suggest that NMN administration augments NK cell cytotoxic activity, but not cell number, in a manner dependent on IFN-γ in both young and elderly mice.
烟酰胺单核苷酸（NMN）是烟酰胺腺嘌呤二核苷酸（NAD）的关键中间体，已被证明可改善老年小鼠疾病模型中的各种病理状况。自然杀伤（NK）细胞是重要的先天免疫细胞；然而，它们的功能会随着衰老而下降。在本研究中，我们检测了NMN处理对小鼠NK细胞的影响。腹腔注射NMN可增强年轻和老年B6小鼠以及年轻BALB/c小鼠的NK细胞细胞毒性活性。口服NMN也可增加老年B6和BALB/c小鼠的NK细胞细胞毒性。然而，在NK细胞细胞毒性活性被NMN激活的小鼠中，NK细胞数量并未增加。有趣的是，在IFN-γ缺陷小鼠中，给予NMN并未增强NK细胞细胞毒性活性。这些结果表明，在年轻和老年小鼠中，给予NMN以依赖IFN-γ的方式增强NK细胞细胞毒性活性，但不增加细胞数量。
