Abstract

Objectives/Hypothesis. To determine if laryngopharyngeal reflux alters mucin gene expression in laryngeal mucosa. Methods. In situ hybridization was employed to study the expression of the 8 well-characterised mucin genes MUC1-4, 5AC, 5B, 6, and 7 in reflux laryngeal mucosa from laryngeal ventricles, posterior commissures, and vocal folds compared to control/normal laryngeal mucosa. Results. MUC1-5 genes are expressed in normal and reflux laryngeal mucosa. MUC1, 3 and 4 are expressed in respiratory and squamous mucosa whereas MUC2 and 5AC are expressed in respiratory mucosa only. MUC3, 4 and 5AC are downregulated in reflux mucosa. MUC5AC expression is significantly reduced in the 3 mucosal sites and when mucosal type was taken into account, this remains significant in combined laryngeal and ventricular mucosa only. Conclusions. MUC3, 4 and 5AC expression is downregulated in laryngopharyngeal reflux. This may be due to laryngeal mucosal metaplasia and/or alteration of mucin gene expression in the preexisting mucosa. Altered mucin gene expression might predispose laryngeal mucosa to the damaging effect of reflux.

Highlights

  • Mucin gene expression is tissue specific in order to afford protection for the relevant mucosa

  • This study aims to investigate mucin gene expression in laryngeal mucosa of Laryngopharyngeal reflux (LPR) patients in contrast to control/normal laryngeal mucosa

  • Squamous metaplasia was noted in reflux laryngeal mucosa from the 3 locations

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Summary

Introduction

Mucin gene expression is tissue specific in order to afford protection for the relevant mucosa In certain conditions such as inflammation, metaplasia, and neoplasia, mucin gene expression patterns can be altered through changes in the nature of the mucosal tissue. An example is Barrett’s oesophageal metaplasia when lower oesophageal mucosa changes from squamous to gastrointestinal mucosa containing mucus secreting cells [1]. This appears to result from repetitive insult to oesophageal mucosa by gastric refluxate leading to altered mucin expression from normal membrane-bound mucins and submucosal gland secretory mucins to the secretory gelforming mucins similar to those found in the gastrointestinal tract. Laryngopharyngeal reflux (LPR) has become more commonly attributed as an etiology of many upper airway disorders for which there has previously been no known aetiology

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