The senescence-accelerated mouse shows aging-related defects in cellular but not humoral immunity against influenza virus infection.
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.
Dong
L
L
Department of Microbiology, Fukui Medical University School of Medicine, Fukui, Japan.
Mori
I
I
Hossain
M J
MJ
Kimura
Y
Y
D000375:Aging / Q000276:immunology*; D000818:Animals; D000917:Antibody Formation; D016516:CD4-CD8 Ratio; D016207:Cytokines / Q000096:biosynthesis; D004198:Disease Susceptibility; D007111:Immunity, Cellular; D009980:Influenza A virus / Q000276:immunology*; D007694:Killer Cells, Natural / Q000276:immunology; D051379:Mice; D008806:Mice, Inbred AKR; D009976:Orthomyxoviridae Infections / Q000276:immunology*; D013154:Spleen / Q000166:cytology / Q000276:immunology; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology; D018417:Th1 Cells / Q000276:immunology; D013950:Thymus Gland / Q000166:cytology / Q000276:immunology
D016207:Cytokines