Johnson A P, Taylor-Robinson D, Slavin G
Br J Vener Dis. 1977 Feb;53(1):26-30. doi: 10.1136/sti.53.1.26.
Gonococci of colony type 1 were introduced by intranasal inoculation into the lungs of mice in an attempt to produce infection. The organisms were eliminated from the three strains of mice used within 24 hours of challenge. Cyclophosphamide treatment of mice failed to render them susceptible although the organisms disappeared more slowly. The lungs of immunologically normal animals that had received either viable or heat-killed gonococci were acutely inflamed with infiltration of bronchioles and alveoli by polymorphonuclear and mononuclear leucocytes. Most of the changes had resolved after about four days. In cyclophosphamide-treated mice pulmonary infiltration by polymorphonuclear leucocytes was not evident, suggesting that these cells were not primarily responsible for the clearance of the gonococci. Despite the failure to produce a sustained infection, this model may be valuable for studying the local inflammatory effect of gonococcal endotoxin.
将1型菌落的淋球菌通过鼻内接种引入小鼠肺部，试图引发感染。在攻击后24小时内，所用的三株小鼠体内的这些微生物均被清除。对小鼠进行环磷酰胺治疗未能使其易感，尽管微生物消失得更慢。接受活的或热灭活淋球菌的免疫正常动物的肺部出现急性炎症，细支气管和肺泡有多形核白细胞和单核白细胞浸润。大约四天后，大多数变化已消退。在环磷酰胺治疗的小鼠中，多形核白细胞的肺部浸润不明显，这表明这些细胞并非淋球菌清除的主要原因。尽管未能产生持续性感染，但该模型对于研究淋球菌内毒素的局部炎症作用可能有价值。
