Lefford M J, Amell L, Warner S
Infect Immun. 1978 Dec;22(3):746-51. doi: 10.1128/iai.22.3.746-751.1978.
After implantation of approximately 10(3) Listeria monocytogenes organisms into the lungs, mice develop an acute pneumonitis with dissemination of infection to a mediastinal lymph node (MedLN), liver, and spleen. The infections in a MedLN and spleen resolve in approximately 7 days, but the lung infection persists for a few days longer. Pneumonitis is accompanied by a lymphoproliferative response in a MedLN and spleen, and immunity to Listeria is conferred adoptively with MedLN and spleen cells but not with mesenteric lymph node cells. Although the spleen appears to be the major repository of sensitized lymphocytes, splenectomized mice combat Listeria pneumonitis as effectively as normal mice. It is concluded that the induction of immunity to lung infection with L. monocytogenes is efficient and that the cause for the rather protracted pneumonitis is due to a defect in the expression of the cell-mediated immunity effector mechanism.
将约10³个单核细胞增生李斯特菌接种到小鼠肺部后,小鼠会发展为急性肺炎,感染扩散至纵隔淋巴结(MedLN)、肝脏和脾脏。纵隔淋巴结和脾脏中的感染大约在7天内消退,但肺部感染会持续更长几天。肺炎伴随着纵隔淋巴结和脾脏中的淋巴细胞增殖反应,对李斯特菌的免疫通过纵隔淋巴结和脾细胞进行过继性传递,但肠系膜淋巴结细胞则不能。尽管脾脏似乎是致敏淋巴细胞的主要储存库,但脾切除的小鼠抵抗李斯特菌肺炎的效果与正常小鼠一样有效。得出的结论是,对单核细胞增生李斯特菌肺部感染的免疫诱导是有效的,而肺炎迁延不愈的原因是细胞介导免疫效应机制的表达存在缺陷。