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Variation in the quantity and character of middle ear secretions and specifically mucin production is known to be important in the pathophysiology of otitis media [1]. Mucin production can be stimulated by inflammatory conditions [2], and the adenoid, as a bacterial reservoir, can propagate this inflammatory state [3]. Further study of the relationship between inflammatory cytokines, mucin production, and mucin gene expression will provide a better understanding of the pathophysiologic mechanisms in otitis media.

Nine distinct human mucins have been identified, and are differentially expressed according to tissue type. Tracheobronchial epithelium has been shown to express MUC 5AC [4], Eustachian tube epithelium expresses MUC 5AC and MUC 5B [5], and the middle ear epithelium expresses mainly MUC 5B. We wanted to determine whether the MUC 5AC mucin gene was differentially expressed in adenoid tissue among individuals with and without otitis media with effusion.

Specimen collection and research protocol was approved by the research and publications committee and Human Rights Review Board of the Children's Hospital of Wisconsin. Total RNA isolated using Qiagen mini RNeasy columns from homogenated adenoid specimens was incubated with DNAse, precipitated, and quantitated by spectrometry. Three micrograms of DNA free RNA was used in positive and negative reverse-transcriptase reactions, and subsequent template used to perform quantitative radioactive PCR amplification of MUC 5AC and GAPDH targets. MUC 5AC expression was normalized to GAPDH amplification.

Fourteen specimens were collected, eight from children undergoing adenoidectomy for OME and six from children undergoing adenoidectomy for upper airway obstruction (UAO). Individuals with both diagnoses were excluded. These groups were balanced in age and sex distribution. Quantitative RT-PCR of mucin expression demonstrated a normalized value of 44.8 au±53.8 for MUC 5AC in children with OME and 159.8 au±97.2 for MUC 5AC in children without OME (p=0.02). GAPDH amplification was equivalent between groups, and reverse-transcriptase negative reactions showed no amplification. See Figs. 1 and 2.

Mucins play multiple roles in the physiology of the nasopharynx and middle ear. In this study we show that MUC 5AC is differentially expressed in the adenoid tissue of children suffering from OME compared to children with UAO. Although mucin accumulation in the middle ear causes morbidity (hearing loss) in children, our results suggest there is less MUC 5AC expression in the adenoids of children with OME as compared to those without OME. Specifically, children with OME express MUC 5AC approximately 3.5 fold less than children with UAO (p=0.02). Although otitis and glue ear are traditionally thought of as states of excess mucin, this study suggests that this relationship may be more complicated, at least with respect to mucin expression in the nasopharynx. It has been demonstrated that nasopharyngeal mucin is important in bacterial adherence in the nasopharynx, impacting colonization and host defenses and acute and chronic infectious processes in this area [6]. Thus, it is likely that either excess or deficiency of specific mucin types may impact an individual's response to pathogens, affect Eustachian tube function, middle ear inflammation and acute and chronic otitis media. Future studies will look at other mucin sub-types and their expression patterns in the nasopharynx and the potential relationship of this expression to otitis media.