Induction of mucin and adhesion molecules in middle ear mucosa.

We hypothesized that inflammation molecules induce the secretory hyperplasia characteristic of otitis media with effusion (OME). The purpose of the present study was to compare the location of inflammation molecules and mucin in the middle ear mucosa of both normal and OME ears. OME was created by bisection of the tensor veli palatini muscle in germ-free rabbits, and the development of middle ear effusion was confirmed by otomicroscopy and tympanometry. Ventilation tubes (VTs) were inserted in half of the ears. The animals were decapitated after 8 weeks, and serial sections of the middle ear mucosae were either periodic acid-Schiff (PAS)-stained or stained immunohistochemically for inflammation molecules or mucins. The length of stained epithelium was measured and related to the total epithelial length. There was a striking resemblance between mucin-type MUC5B- and PAS-positive epithelium and areas positive for the chemoattractant inflammation molecules intercellular adhesion molecule-1 (ICAM-1) and RANTES (reacted upon activation, normal T expressed and secreted). The percentages of ICAM-1- and PAS-stained epithelium were significantly higher in OME ears than in normal ears. OME ears treated with VTs also contained significantly more PAS-positive epithelium than normal ears, but less than OME ears. Based on the spatial and temporal coincidence between ICAM-1 and mucin, it is suggested that: (i) inflammation may initiate and maintain the hypersecretory state of the middle ear mucosa which is presumably responsible for the chronicity of OME; and (ii) that MUC5B is a major mucin component of OME effusions.