[Influenza A virus-induced mucociliary dysfunction of tubotympanum]

There is amount of epidemiologic, clinical and laboratory evidence to document that viral infection is involved in otitis media with effusion (OME). However, few studies have demonstrated the direct influence of viruses on the tubotympanum. The purpose of this study is to establish the effect of influenza A virus invaded in the tubotympanum, in an attempt to elucidate the possible mechanism by which the virus contributes to the pathogenesis of OME. 80 guinea pigs with normal otoscopic findings were inoculated with 0.2ml suspension of influenza A (3.3 x 10(8)PFU/ml) into their tympanic cavities through their tympanic membranes. To serve as controls, the same number of guinea pigs were injected with 0.2ml of physiologic saline solution into their tympanic cavities. At 3, 7, 14, and 28 days postinoculation, they were used for examination of the mucociliary function. Middle ear effusions were observed only in the animals inoculated with the virus. Mucociliary dysfunction was observed only in the animals inoculated with the virus. The ciliary activity in the bulla was declined at any time examined. On the other hand, the ciliary activity in the eustachian tube and the tympanic orifice was slightly lowered between 7 and 14 days, but the level was not different from that of the control. However, the number of active ciliated cells (showing more than 500 beats/min) was significantly smaller than that of the control. The mucociliary clearance time of the tubotympanum was more prolonged than that of the control at 3, 7, and 14 days, and returned to the control level at 28 days. A variety of morphologic changes were observed in the tubotympanum treated with the virus. Major pathologies observed included a general inflammatory cell infiltration, vacuolation and other degeneration of ciliated cells, and vascular damage and increased vascular permeability. Regeneration of cilia or ciliated cells followed the degeneration, which included an increased number of basal cells and new formed centrioles. However, the viral infection had an influence on the epithelial cells with new centrioles. Our study has demonstrated that viral infection could evoke mucociliary dysfunction of the tubotympanum and create an increased susceptibility to bacteria. Therefore, viral infection could enhance bacterial infectious process in the tubotympanum. Through the failure viruses could contribute to the occurrence of OME.