Department of Medicine and the Oscar Johnson Institute for Medical Research, Washington University School of Medicine, St. Louis.
J Exp Med. 1950 Feb 28;91(3):245-60. doi: 10.1084/jem.91.3.245.
Pulmonary edema is a component of the fully developed influenza viral lesion in the mouse. Mice with experimental pulmonary fluid have an increased susceptibility to inhaled pneumococci and under these circumstances the organisms grow in the lung and produce the lesion of bacterial pneumonia. The presence of pulmonary edema in the lesion due to the influenza virus in the lung of the mouse appears to account adequately for the previous observation that inhaled pneumococci grow in the influenza viral lesion. Mice dying of pneumococcal septicemia after inhaling fine droplets containing this organism do not have pneumonia. The delay in migration of polymorphonuclear leucocytes into the lung after injection of pneumococci suspended in serum is an important factor in susceptibility to infection since it allows ample time for pneumococci to grow in the pulmonary fluid. The slow phagocytic action of pulmonary macrophages likewise permits growth of pneumococci. Conditions in human beings that are known to be complicated by pulmonary edema are also known to be associated with increased susceptibility to secondary bacterial pneumonia.
肺水肿是小鼠完全发育的流感病毒病变的一个组成部分。患有实验性肺水肿的小鼠对吸入性肺炎球菌的易感性增加，在这种情况下，这些生物体在肺部生长并产生细菌性肺炎的病变。流感病毒在小鼠肺部病变中出现肺水肿，似乎足以说明以前观察到的吸入性肺炎球菌在流感病毒病变中生长的现象。吸入含有这种生物体的细飞沫后死于肺炎球菌败血症的小鼠没有肺炎。肺炎球菌混悬液注入后，多形核白细胞向肺部迁移的延迟是易感性的一个重要因素，因为它为肺炎球菌在肺液中生长提供了充足的时间。肺巨噬细胞的缓慢吞噬作用同样允许肺炎球菌生长。已知肺水肿会使人类病情复杂化的情况，也与继发性细菌性肺炎的易感性增加有关。
