HARFORD C G, HAMLIN A
J Exp Med. 1952 Feb;95(2):173-90. doi: 10.1084/jem.95.2.173.
In order to determine the effect of infection with influenza virus on bronchial cilia of the mouse, ciliary beat has been visualized directly by microscopic examination of the bronchi in slices of fresh lung. Cilia have been shown also in sections of fixed tissue by the use of special silver staining methods. The results have shown persistence of the cilia in spite of severe viral infection and indicate that the lowered resistance to secondary pneumococcal infection which occurs in influenzal pneumonia of the mouse is not due to interference with the ciliary mechanism. By a process of exclusion, the findings give further support to the theory that lowered resistance to pneumococcal infection in influenzal pneumonia is due to edema fluid in the viral lesion furnishing a culture medium for inhaled pneumococci. A widely used method for evaluation of ciliary activity on respiratory epithelia has been the microscopic observation of wave-like movements in reflected light. This activity was observed readily in the bronchi of mice but evidence was obtained showing that at this site it was due to something other than ciliary beat. Further histopathologic observations were made in order to define the lesion of the bronchial epithelium that would permit sparing of ciliated cells. In addition to usual techniques, mice were injected with colchicine for estimation of the rate of cellular proliferation and were exposed to a large dose of roentgen rays to eliminate polymorphonuclear leucocytes. Stains for mucous and for mitochondria were done also. The evidence obtained favors the theory that the viral infection does not destroy any of the cells of the bronchial epithelium. Inclusion bodies were found in the cytoplasm, making it seem likely instead that viral particles grow in colony-like aggregations and that liberation of virus into the lumen takes place not only by simple extrusion of inclusions but also by detachment of inclusion-laden globular portions of the cytoplasm.
为了确定感染流感病毒对小鼠支气管纤毛的影响，通过对新鲜肺切片中的支气管进行显微镜检查，直接观察到了纤毛摆动。使用特殊的银染色方法，在固定组织切片中也显示出了纤毛。结果表明，尽管存在严重的病毒感染，纤毛仍持续存在，这表明小鼠流感性肺炎中对继发性肺炎球菌感染的抵抗力降低并非由于纤毛机制受到干扰。通过排除法，这些发现进一步支持了以下理论：流感性肺炎中对肺炎球菌感染抵抗力降低是由于病毒病变中的水肿液为吸入的肺炎球菌提供了培养基。一种广泛用于评估呼吸道上皮纤毛活性的方法是在反射光下显微镜观察波浪状运动。在小鼠支气管中很容易观察到这种活动，但有证据表明，在这个部位，它是由纤毛摆动以外的其他因素引起的。为了确定能使纤毛细胞幸免的支气管上皮病变，进行了进一步的组织病理学观察。除了常规技术外，给小鼠注射秋水仙碱以估计细胞增殖速率，并使其暴露于大剂量X射线下以消除多形核白细胞。还进行了黏液和线粒体染色。所获得的证据支持了病毒感染不会破坏支气管上皮任何细胞的理论。在细胞质中发现了包涵体，这似乎表明病毒颗粒以菌落样聚集的形式生长，并且病毒释放到管腔中不仅通过包涵体的简单挤出，还通过含有包涵体的细胞质球状部分的脱离。
