Induction of mucin and adhesion molecules in middle ear mucosa

We hypothesized that inflammation molecules induce the secretory hyperplasi a characteristic of otitis media with effusion (OME). The purpose of the pr esent study was to compare the location of inflammation molecules and mucin in the middle car mucosa of both normal and OME ears. OME was created by b isection of the tensor veli palatini muscle in germ-free rabbits, and the d evelopment of middle ear effusion was confirmed by otomicroscopy and tympan ometry, Ventilation tubes (VTs) were inserted in half of the cars. The anim als were decapitated after 8 weeks, and serial sections of the middle ear m ucosae were either periodic acid-Schiff (PAS)-stained or stained immunohist ochemically for inflammation molecules or mucins. The length of stained epi thelium was measured and related to the total epithelial length, There was a striking resemblance between mucin-type MUC5B- and PAS-positive epitheliu m and areas positive for the chemoattractant inflammation molecules interce llular adhesion molecule-1 (ICAM-1) and RANTES (reacted upon activation, no rmal T expressed and secreted). The percentages of ICAM-1- and PAS-stained epithelium were significantly higher in OME cars than in normal ears. OME e ars treated with VTs also contained significantly more PAS-positive epithel ium than normal ears, but less than OME ears. Based on the spatial and temp oral coincidence between ICAM-1 and mucin, it is suggested that: (i) inflam mation may initiate and maintain the hypersecretory state of the middle car mucosa which is presumably responsible for the chronicity of OME; and (ii) that MUM is a major mucin component of OME effusions.