Acute starvation protects mice against Listeria monocytogenes.
Acute starvation protects mice against Listeria monocytogenes.
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DOI：
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发表时间：
1980-06
影响因子：
3.1
通讯作者：
E. Wing;J. Young
中科院分区：
文献类型：
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作者：
E. Wing;J. Young
我们研究了饥饿对小鼠单核细胞增生李斯特菌感染过程的影响。小鼠饥饿24、48或72 h后接种致死剂量的L.单核细胞增多症显示出比未饥饿的小鼠显著更低的死亡率（即，喂养的小鼠）。饥饿48或72 h的保护作用在饥饿期后立即开始，并持续至少48 h。饥饿的感染小鼠体内的L.在感染后2、3和4天，它们的脾脏中单核细胞增多症细胞比喂养的小鼠多。无论是T淋巴细胞功能的变化，也没有血清因素似乎是负责的保护作用。对L.单核细胞增多症抗原在饥饿小鼠中比在进食小鼠中小。非免疫饥饿小鼠脾细胞的连续转移不能保护L.单核细胞增多症进一步的研究表明，饥饿小鼠的血清不抑制L。单核细胞增多症，也不能转移对L。单核细胞增生正常小鼠。相反，与对照小鼠的巨噬细胞相比，饥饿小鼠的腹腔巨噬细胞抑制P815肿瘤细胞的脱氧核糖核酸合成。因此，饥饿小鼠对L.单核细胞增多症最有可能是由于非特异性因素，其中之一可能是巨噬细胞的活化。
We investigated the effect of starvation on the course of Listeria monocytogenes infections in mice. Mice starved for 24, 48, or 72 h and then inoculated with a lethal dose of L. monocytogenes showed significantly less mortality than mice not starved (i.e., fed mice). The protective effect of 48 or 72 h of starvation began immediately after the starvation period and persisted for at least 48 h. Starved, infected mice had significantly fewer L. monocytogenes cells in their spleens 2, 3, and 4 days after infection than did fed mice. Neither changes in T-lymphocyte function nor serum factors appeared to be responsible for the protective effect. Delayed hypersensitivity responses to L. monocytogenes antigen were smaller in starved mice than in fed mice. Adoptive transfer of spleen cells from nonimmune starved mice did not protect against L. monocytogenes. Additional studies indicated that the serum of starved mice did not inhibit multiplication of L. monocytogenes in vitro, nor was it able to transfer protection against L. monocytogenes to normal mice. In contrast, peritoneal macrophages from starved mice inhibited deoxyribonucleic acid synthesis of P815 tumor cells compared with macrophages from control mice. Therefore, the resistance of starved mice to L. monocytogenes is most likely due to nonspecific factors, one of which may be activation of macrophages.