Wing E J, Young J B
Infect Immun. 1980 Jun;28(3):771-6. doi: 10.1128/iai.28.3.771-776.1980.
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.
我们研究了饥饿对小鼠单核细胞增生李斯特菌感染病程的影响。饥饿24、48或72小时后接种致死剂量单核细胞增生李斯特菌的小鼠，其死亡率显著低于未饥饿的小鼠（即喂食的小鼠）。饥饿48或72小时的保护作用在饥饿期结束后立即开始，并持续至少48小时。感染后2、3和4天，饥饿且感染的小鼠脾脏中的单核细胞增生李斯特菌细胞数量明显少于喂食的小鼠。T淋巴细胞功能的变化和血清因子似乎都与这种保护作用无关。饥饿小鼠对单核细胞增生李斯特菌抗原的迟发型超敏反应比喂食小鼠小。将未免疫的饥饿小鼠的脾细胞进行过继转移并不能预防单核细胞增生李斯特菌感染。进一步的研究表明，饥饿小鼠的血清在体外不能抑制单核细胞增生李斯特菌的增殖，也不能将对单核细胞增生李斯特菌的保护作用转移给正常小鼠。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了P815肿瘤细胞的脱氧核糖核酸合成。因此，饥饿小鼠对单核细胞增生李斯特菌的抵抗力很可能归因于非特异性因素，其中之一可能是巨噬细胞的激活。
