Abstract
A key issue in otitis media is mucous cell metaplasia which is responsible for mucous hypersecretion and persistence of the disease. However, little is known about the molecular mechanisms of mucous cell metaplasia in otitis media. Numerous studies of intestinal epithelial homeostasis have shown that Atonal homolog 1 (Atoh1), a basic helix-loop-helix (bHLH) transcription factor, is essential for the intestinal goblet cell differentiation. On the other hand, SAM-pointed domain-containing Ets transcription factor (SPDEF), a member of the “Ets” transcription factor family, has been reported to trigger the mucous cell metaplasia of pulmonary infectious diseases or athsma. Recent studies have demonstrated the relation of these factors, that is, Spdef functions downstream of Atoh1. We could take the adventages of these findings for the study of otitis media because both middle ear and pulmonary epithelia belong to the same respiratory tract. Atoh1 and SPDEF could be the therapeutic targets for otitis media associated with mucous cell metaplasia which is frequently considered “intractable” in the clinical settings.
Highlights
Mucous Cell Metaplasia in Intractable Otitis MediaOne of the most characteristic features of intractable otitis media is mucous hypersecretion
A key issue in otitis media is mucous cell metaplasia which is responsible for mucous hypersecretion and persistence of the disease
Accumulated pieces of evidence indicate that Spdef functions downstream of Atonal homolog 1 (Atoh1), and this is mediated by another transcription factor, growth-factor-independent 1 (GFI1), which is normally expressed in the both Paneth and goblet cells (Figure 2)
Summary
One of the most characteristic features of intractable otitis media is mucous hypersecretion. The increase of goblet cells and decrease of ciliated cells are reported in the rat model of otitis media with effusion induced by the endotoxin plus Eustachian tube obstruction [4]. These findings suggest that the ciliated cells convert to goblet cells under the pathological conditions via a biologic process called cell transdifferentiation. Under pathological conditions inducing mucous cell metaplasia, an increased goblet cell population in the mucosa produces excessive mucins, while the loss of ciliated cells in the mucosa results in the dysfunction of the mucociliary transport system, leading to subsequent problems such as fluid accumulation and repeated infections. It is necessary to understand the disease mechanism of mucous cell metaplasia in order to cure this intractable illness
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