Interleukin-4 (IL-4) may play a central role in the IgE synthesis system, the development of Th-2-like cells, and co-ordination as well as the persistence of airway inflammatory process in allergic disorders. Therefore, IL-4 plays a key role in airway allergic disorders. This study aimed at investigating the serum concentrations of IL-4 in patients with perennial allergic rhinitis, with special reference to the possible changes and the clinical relevance following long-term immunotherapy. The study has demonstrated that the serum level of IL-4 in allergic rhinitis patients before immunotherapy is significantly higher than that in non-atopic individuals. However, the serum IL-4 level in allergic rhinitis patients did not decrease following anti-allergic medications but significantly decreased following immunotherapy. The percentage decrease in IL-4 was correlated significantly with the percentage decrease in specific IgE antibodies following long-term immunotherapy. Immunotherapy also significantly decreased specific IgE anti-bodies, but this reduction in specific IgE antibodies was not significantly correlated with the clinical improvement. In contrast, the percentage decrease in serum IL-4 was significantly correlated with the percentage decrease in symptomatic scores. The authors interpret these data to mean that immunotherapy alters T-cell cytokine profiles in the long-term, and a decline of IL-4 following immunotherapy could modulate not only production of specific IgE antibodies but also inflammatory cellular events, leading to symptomatic relief in allergic rhinitis.

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Influenza A virus-induced otitis media and mucociliary dysfunction in the guinea pig. Acta Otolaryngol (Stockh) 1991; Suppl. 135-1 48.There is much epidemiologic, clinical and laboratory evidence that viral infection is involved in otitis media with effusion (OME). However, few studies have demonstrated any direct influence of viruses on the tubotympanum. The purpose of this study was to establish the effect of influenza A virus having invaded the tubotympanum and so elucidate the possible mechanism by which this virus contributes to the pathogenesis of OME. Eighty guinea pigs with normal otoscopic findings were inoculated with 0.2 ml suspension of influenza A ( 3 . 3~ 10' PFU/ml) into the tympanic cavity through the tympanic membrane. To serve as controls, the same number of guinea pigs were injected with 0.2 ml of physiologic saline solution into the tympanic cavity. At 3, 7, 14, and 28 days postinoculation, they were used for examination of the mucociliary function. Middle ear effusions as well as mucociliary dysfunction were 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 controls. However, the number of active ciliated cells (showing more than 500 beatshin) was significantly smaller than that of the controls. The mucociliary clearance time of the tubotympanum was more prolonged than that of the controls at 3, 7, and 14 days, and returned to the control level at 28 days. A variety of morphological changes were observed in the tubotympanum treated with the virus. Major pathologies observed included 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 newly formed centrioles. However, the viral infection also affected the epithelial cells with new centrioles. Our study demonstrates that viral infection can evoke mucociliary dysfunction of the tubotympanum and create increased susceptibility to bacteria. Therefore, viral infection may enhance bacterial infectious processes in the tubotympanu thereby contributing to the occurrence of OME. Key words: influenza A , Otitis media. Mucociliary dysfunction, ciliaty activity. Staphylococcus pneumoniae whereas the incidence of acute otitis media was over 62 Yo when the middle ear deflated. When the nasopharynxes were instilled with S. pneumoniae together with influenza A virus, the incidence of otitis media was 67%. A follow-up study has documented that influenza A virus immediately destructs the epithelium of the Eustachian Acta Otolaryngol Downloaded from informahealthcare.com by Nyu Medical Center on 06/29/15For personal use only.

Y . Histamine-induced mucociliary dysfunction and otitis media with effusion. Acta Otolaryngol (Stockh) I991 ; Suppl.Histamine, which has been found in middle ear effusions, is a potent pharmacological mediator released at an early stage of allergic reactions or general inflammatory process, increasing permeability of small blood vessels. Histamine might be involved in the origin and chronicity of middle ear effusions. In this study we studied the effect of histamine on the mucociliary function. First we examined the effect of histamine and its HI and H, blockers on the ciliary activity in the middle ear.M of histamine deteriorated ciliary activity; however, at lower concentrations ciliostimulatory effects were demonstrated for histamine (between M and M). Such ciliostimulatory effects were not affected by diphenhydramine (H,-blocker) but were reduced by cimetidine (H,-blocker). Thus histamine stimulates ciliary activity by combining with H,-receptor. Intratympanic injection of M of histamine induced accumulation of middle ear effusions (MEEs). The volume of MEEs was largest at 1 day postinjection when its mucociliary clearance time was longest. Then the mucociliary clearance time became shorter, but it was still significantly longer than that of the control animal. Ciliary activity in the tubotympanum showed no recovery through the observation period. On the other hand, intratympanic injection of M of histamine produced MEEs at 1 and 3 days postinjection when the mucociliary clearance time was longer than that of the control group. At 8 days, when most ears did not demonstrate MEEs, the mucociliary clearance time and ciliary activity in the Eustachian tube and tympanic orifice reached the level of the control group. Our present study demonstrates that histamine can induce mucociliary dysfunction of the tubotympanum resulting in middle ear effusions, and that cilia, especially those present in the tube and the tympanic orifice, have a significant role in eliminating middle ear effusions.