Yoshida R, Sato K, Yoo Y C, Yoshimatsu K, Tamura M, Ishihara C, Arikawa J, Azuma I
Institute of Immunological Science, Hokkaido University, Sapporo, Japan.
Immunopharmacology. 1994 Sep-Oct;28(2):153-61. doi: 10.1016/0162-3109(94)90031-0.
DT-5461 enhanced host resistance to Sendai virus infection in mice. Intranasal (i.n.) administration of 200 micrograms of DT-5461 per mouse 3 days before infection was the most effective administration route, dose and timing. DT-5461 enhanced the cytotoxicity of murine natural killer (NK) cells. In addition, DT-5461 activated murine peritoneal macrophages, resulted in augmented of cytotoxicity and the induction of tumor necrosis factor-alpha (TNF-alpha). Therefore, these immunomodulating activities presented by DT-5461 caused protection against Sendai virus infection.
DT-5461增强了小鼠对仙台病毒感染的抵抗力。在感染前3天,每只小鼠经鼻内(i.n.)给予200微克DT-5461是最有效的给药途径、剂量和时间。DT-5461增强了小鼠自然杀伤(NK)细胞的细胞毒性。此外,DT-5461激活了小鼠腹腔巨噬细胞,导致细胞毒性增强和肿瘤坏死因子-α(TNF-α)的诱导。因此,DT-5461呈现的这些免疫调节活性导致了对仙台病毒感染的保护作用。