[Inflammation and acute otitis media]

1. EPITHELIUM OF THE MIDDLE EAR: The middle ear has a respiratory type epithelium. The mucus is produced by mucosal and by submucosal cells in the Eustachian tube. 2. LYMPHOID TISSUE: The defensive barrier of the mucosa is potentialized by lymphoid tissue in the middle ear that produces a local specific immune response. Bacterial and viral antigens can induce an inflammatory reaction. 3. TUBOTYMAPNIC CAVITIES: The humoral immune system (B lymphocytes) secreting IgG, IgA and IgM) and cell mediated response (T lymphocytes) are active in the tubotympanic cavities. 4. MAST CELLS: Present in contact with vessels and nervous fibers of the tubotympanic chorion, mast cells are activated by IgE linkage to antigens, leading to local allergic inflammatory phenomena with production of histamine, C leukotrienes, platelet activating factor (PAF) and cytokines. 5. MAINTAINING OPEN CAVITIES: During the inflammatory reaction, mucus-secreting cells are stimulated and their glycoprotein secretions are modified. Since the middle ear epithelium has a water-absorption action contributing to aeration of the middle ear cavities. 6. CYTOKINE RESPONSE: During acute middle ear otitis, cytokines secreted in response to bacterial and viral lipopolysaccharides include tumor necrosis factor alpha (TNFa) which plays a crucial role: induction of fibroblast proliferation, activation of polymorphonuclears, inhibition of vascular endothelial tissue and B lymphocytes. It facilitates healing of the middle ear infection, but an also induced pathological lesions in case of incomplete repair. 7. BACTERIAL FLORA: Haemophilus influence, Branhamella catarrhalis, and Streptococcus pneumoniae colonize the respiratory epithelium of the middle ear via the Eustachian tube, generally after viral infection. 8. GLUCOCORTICOIDS: Administered before injection of a bacterial endotoxin, glucocorticoids significantly reduce inflammatory phenomena in acute otitis induced in rat models. In acute middle ear models in the guinea pig, corticosteroids reduce lipoperoxidation; free radicals are the cause of the persistence of inflammation in the acute middle ear. 9. NEUTROPHIL MIGRATION: Antibodies blocking cell adhesion molecules (CAM), or instance antiCD11 B and antiCT 18, inhibit polymorphonuclear migration, and could be very useful for the treatment of acute middle ear infection. Use of prostaglandin inhibitors does not significantly reduce the risk of residual effusion at 10 and 30 days after the acute episode. 10.

There is a significant body of scientific evidence proving the efficacy of combining antiinflammatory drugs and antibiotics for first line treatment of middle ear infection to prevent seromucosal otitis.