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.

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