幼龄和老年小鼠在流感侵袭后的肺免疫反应。

B S Bender, S F Taylor, D S Zander, R Cottey
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摘要

在流感攻击后,老年小鼠有延长的病毒脱落,这与较低的脾细胞毒性T淋巴细胞(CTL)活性相关。为了评估年龄相关的肺细胞介导的流感免疫反应,在呼吸道感染非致死性流感病毒A/PC/1/73 (H3N2)后的不同天,从年轻和老年小鼠中获得肺淋巴细胞。在幼鼠中,肺部CTL活性在感染后第7天达到48% +/- 2%的峰值。老年小鼠肺CTL活性在1天后达到峰值,约为活性的一半(24% +/- 5%)。在两个年龄组中,从肺中恢复的细胞大部分是CD3+、CD8+ T细胞。肺部的组织学检查显示,老年小鼠的炎症明显少于年轻小鼠。因此,在流感攻击后,大量淋巴细胞涌入年轻和年老小鼠的肺部,但年轻小鼠的细胞在每个细胞的基础上更活跃。在进一步的实验中,用毒性更强的流感毒株攻击幼鼠,其死亡率高于老龄鼠。因此,幼龄动物较高的CTL活性导致更快的病毒清除,但这可能对宿主有代价——即更多的免疫病理损伤。
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Pulmonary immune response of young and aged mice after influenza challenge.

After influenza challenge, aged mice have prolonged viral shedding that correlates with lower splenic cytotoxic T lymphocyte (CTL) activity. To evaluate the age-related pulmonary cell-mediated immune response to influenza, pulmonary lymphocytes were obtained from young and aged mice at various days after respiratory tract infection with nonlethal influenza A/PC/1/73 (H3N2) virus. In young mice, pulmonary CTL activity peaked at 48% +/- 2% on day 7 after infection. Pulmonary CTL activity peaked 1 day later in aged mice and at about half the activity (24% +/- 5%). The majority of the cells recovered from the lungs in both age groups were CD3+, CD8+ T cells. Histologic examination of the lungs revealed that aged mice had significantly less inflammation than young mice. Therefore, after influenza challenge there was a large influx of lymphocytes into the lungs of both young and aged mice, but the cells from young mice were more active on a per-cell basis. In a further experiment, challenge with a more virulent strain of influenza produced higher mortality in young mice than in aged mice. Thus the higher CTL activity of young animals leads to more rapid virai clearance, but this may be at a price to the host--that is, more immunopathologic damage.

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