Mucin Production and Mucous Cell Metaplasia in Otitis Media

Jizhen Lin,Xiaohua Hu,Quan-An Zhang,Joseph E Kerschner,Per Caye-Thomasen,Ling Feng,Jianmin Huang,Yoshihisa Nakamura,Tetsuya Tono,Shengnan Ye

doi:10.1155/2012/745325

Abstract

Otitis media (OM) with mucoid effusion, characterized by mucous cell metaplasia/hyperplasia in the middle ear cleft and thick fluid accumulation in the middle ear cavity, is a subtype of OM which frequently leads to chronic OM in young children. Multiple factors are involved in the developmental process of OM with mucoid effusion, especially disorders of mucin production resulting from middle ear bacterial infection and Eustachian tube dysfunction. In this review, we will focus on several aspects of this disorder by analyzing the cellular and molecular events such as mucin production and mucous cell differentiation in the middle ear mucosa with OM. In addition, infectious agents, mucin production triggers, and relevant signaling pathways will be discussed.

Highlights

Otitis media (OM) is characterized by the production of mucins in the middle ear mucosa
Otitis media (OM) with mucoid effusion, characterized by mucous cell metaplasia/hyperplasia in the middle ear cleft and thick fluid accumulation in the middle ear cavity, is a subtype of OM which frequently leads to chronic OM in young children
Multiple factors are involved in the developmental process of OM with mucoid effusion, especially disorders of mucin production resulting from middle ear bacterial infection and Eustachian tube dysfunction

Summary

Introduction

Otitis media (OM) is characterized by the production of mucins in the middle ear mucosa. Mucous cell metaplasia/hyperplasia is a pathological term that describes an increased mucous cell population or density in the upper respiratory mucosa upon infections and/or other stimuli. It is usually determined by histochemical examination with Alcian Blue-Periodic Acid Schiff (ABPAS) stain which identifies large molecular weight glycoproteins (i.e., macroglycoconjugates or macroglycoproteins) in a cell. Peptidoglycan polysaccharides (PGPS, metabolites of S. pneumonae) stimulates epithelial proliferation whereas endotoxin (metabolites of H. influenza) promotes epithelial cell death in cultured middle ear epithelial cells, causing necrosis or apoptosis of the middle ear epithelial cells (Figure 2) This may explain why S. pneumoniae tends to cause mucous cell metaplasia/hyperplasia. It is well recognized that some dead bacterial cell wall fragments or metabolites are sufficient to keep the middle ear mucosa in a state of mucous cell metaplasia/hyperplasia

Mucin Dysregulation in OM

Mucus Gel Composition in OM

Findings

Mucoid Effusion in OM