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首页> 外文期刊>Infection and immunity >Old mice are able to control low-dose aerogenic infections with Mycobacterium tuberculosis.
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Old mice are able to control low-dose aerogenic infections with Mycobacterium tuberculosis.

机译：老年小鼠能够控制结核分枝杆菌的低剂量气源性感染。

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Previous work in this laboratory has led to the development of the hypothesis that the increased susceptibility of old mice to tuberculosis infection reflects a limited ability by immune CD4 mediator cells to accumulate at sites of bacterial implantation. To test this hypothesis with very low dose infections, the present study documented the course of a low-dose aerogenic infection with virulent Mycobacterium tuberculosis Erdman against time in the target organs of young (3-month-old) and old (24-month-old) B6D2F1 hybrid mice. The results of the study indicated that the infection was controlled by the two groups of mice at similar rates, although the bacterial load in the old mice was eventually somewhat higher. Despite these similarities, some subtle differences between the young and old mice were also evident and included evidence of increased hematogenous spread of the infection from the lungs to other organs in the old mice. Interestingly, very poor expression of the cytokine interleukin-12 was observed in the lungs of infected old mice, leading to the hypothesis that the poor CD4 response in such animals could be partially attributed to the lack of this Th1-type, CD4 T-cell-enhancing cytokine. In this regard, treatment of old mice with exogenous interleukin-12 increased resistance and promoted gamma interferon secretion by CD4 T cells from these mice, although the effects were generally modest. These data suggest that old mice possess CD4-independent compensatory mechanisms by which to deal with low-dose pulmonary tuberculosis infections, although such mechanisms are less efficient than those seen in young animals.
机译：在该实验室中的先前工作已导致以下假设的发展：老年小鼠对肺结核感染的敏感性增加反映了免疫CD4介导细胞在细菌植入位点积累的能力有限。为了用极低剂量的感染来检验这一假设，本研究记录了年轻（3个月大）和老年人（24个月大）的目标器官中针对强力结核分枝杆菌Erdman的低剂量气源性感染随时间变化的过程。老）B6D2F1杂交小鼠。研究结果表明，虽然最终小鼠的细菌载量更高，但两组小鼠仍以相似的速度控制感染。尽管有这些相似之处，但在年轻小鼠和老年小鼠之间也存在一些细微的差异，其中包括有证据表明感染的血源性传播从老年小鼠的肺部扩散到其他器官。有趣的是，在受感染的老小鼠的肺中观察到细胞因子白细胞介素12的表达非常差，从而得出这样的假设：此类动物的CD4反应不良可能部分归因于缺乏这种Th1型CD4 T细胞-增强细胞因子。在这方面，用外源白细胞介素12治疗老年小鼠增加了抵抗力，并促进了这些小鼠的CD4 T细胞分泌的γ干扰素，尽管这种作用通常不大。这些数据表明，老年小鼠具有与CD4无关的补偿机制，可通过该机制来应对小剂量肺结核感染，尽管这种机制的效率比幼小动物低。

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