Dong L, Mori I, Hossain M J, Kimura Y
Department of Microbiology, Fukui Medical University School of Medicine, Fukui, Japan.
J Infect Dis. 2000 Aug;182(2):391-6. doi: 10.1086/315727. Epub 2000 Jul 18.
The senescence-accelerated mouse (SAM) strain P1, which has a short life span, was adopted as a murine model for an investigation of the pathogenesis of viral infection in elderly adults. After intranasal inoculation with influenza A virus, the SAM-P1 mice showed a higher rate of mortality, with prolonged virus growth in the lungs. The increased susceptibility was associated with impaired activity of both NK cells and virus-specific cytotoxic T lymphocytes. The production of interferon-gamma and interleukin-12 was significantly restrained, which suggests a partial deficiency of the T helper (Th) 1 cells. In contrast, the immunologic activity of the Th2 cells appeared to be functionally normal, judging from the release of large amounts of interleukin-4 followed by production of appropriate amounts of influenza virus-specific antibody. It is suggested that the elicitation of cellular immunity is an important and effective procedure for protecting the elderly from influenza virus infection.
将寿命较短的衰老加速小鼠（SAM）品系P1用作研究老年人病毒感染发病机制的小鼠模型。甲型流感病毒经鼻内接种后，SAM-P1小鼠死亡率更高，病毒在肺部的生长时间延长。易感性增加与自然杀伤细胞和病毒特异性细胞毒性T淋巴细胞的活性受损有关。γ干扰素和白细胞介素-12的产生受到显著抑制，这表明辅助性T（Th）1细胞部分缺乏。相比之下，从大量白细胞介素-4的释放以及随后产生适量的甲型流感病毒特异性抗体来看，Th2细胞的免疫活性在功能上似乎正常。提示激发细胞免疫是保护老年人免受流感病毒感染的重要且有效措施。
