Adenoids play an important role as an effector site of the mucosal immune system in the upper respiratory tract. IgA immune responses in adenoids are responsible for the clearance of HI from the nasopharynx.

The effect of an antiallergic drug on the evacuation of middle ear effusion (MEE) from the tubotympanum was investigated by means of an animal model with both otitis media with effusion (OME) and allergic rhinitis. Azelastine hydrochloride (AZ), an oral antiallergic drug, was administered and the presence of MEE was investigated. Serous MEE was seen in 12 of the 13 untreated control animals on the 11th day after the experimental OME was induced, whereas MEE was detected in 9 of the 13 animals administered 1 mg/kg of AZ, but only in 4 of the 13 animals administered 2 mg/kg of AZ. In addition, the effect of AZ on MEE production was also examined in an experimental OME animal model without allergic rhinitis. Middle ear effusion was observed in all OME animals that received 2 mg/kg AZ for 5 consecutive days, before and 3 days after the experimental OME was induced. Results of the present study indicate that AZ promotes the evacuation of MEE from the tubotympanum in the OME animal model associated with nasal allergy. These data suggest that an antiallergic drug may contribute to the therapy of OME patients in association with nasal allergy indirectly, by promoting evacuation of MEE due to inhibition of type I allergic reactions in the nasopharynx.

We investigated cellular immunity against Streptococcus pyogenes in human tonsils by measuring antigen-specific immunoglobulin-secreting cells and the production of cytokines from CD4+ T cells in response to M proteins. The incidence of S pyogenes in tonsils was significantly higher in patients with recurrent tonsillitis (RT) than in patients with tonsillar hypertrophy (TH). M protein-specific immunoglobulin A (IgA) and immunoglobulin G spot-forming cells were increased in patients with RT compared with patients with TH. In RT the number of M protein-specific IgA spot-forming cells was significantly greater in the S pyogenes-negative subjects than in the S pyogenes-positive subjects. Proliferation of CD4+ T cells and production of interferon-gamma (IFN-gamma) and interleukins -2, -4, -5, and -6 (IL-2, IL-4, IL-5, and IL-6) from those T cells were observed in response to M protein. The concentrations of IFN-gamma and IL-4 were higher in RT than in TH. These findings suggest that S pyogenes is associated with the pathogenesis of RT and that immune responses against M protein may play an important role in preventing the colonization of this bacteria in tonsils.

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