Laryngeal Epithelial Defenses against Laryngopharyngeal Reflux: Investigations of E-Cadherin, Carbonic Anhydrase Isoenzyme III, and Pepsin

Objectives: This is the third annual report of an international research network studying the cellular impact of laryngopharyngeal reflux (LPR) on laryngeal epithelium. The objective of this study was to investigate the presence of E-cadherin (epithelial cadherin; the intercellular junctional comple...

Full description

Saved in:
Bibliographic Details
Published in:Annals of otology, rhinology & laryngology rhinology & laryngology, 2005-12, Vol.114 (12), p.913-921
Main Authors: Gill, Gulnaz A., Johnston, Nikki, Buda, Andrea, Pignatelli, Massimo, Pearson, Jeffrey, Dettmar, Peter W., Koufman, Jamie
Format: Article
Language:English
Subjects:
Biological and medical sciences
Biopsy
Cadherins - metabolism
Carbonic Anhydrase III - metabolism
Epithelium - pathology
Gastroesophageal Reflux - metabolism
Gastroesophageal Reflux - prevention & control
Humans
Immunohistochemistry
Laryngeal Mucosa - metabolism
Laryngeal Mucosa - pathology
Larynx - metabolism
Larynx - pathology
Larynx - physiopathology
Medical sciences
Otorhinolaryngology. Stomatology
Pepsin A - metabolism
Pharynx - physiopathology
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Objectives: This is the third annual report of an international research network studying the cellular impact of laryngopharyngeal reflux (LPR) on laryngeal epithelium. The objective of this study was to investigate the presence of E-cadherin (epithelial cadherin; the intercellular junctional complex protein) in relation to the presence of (intracellular) pepsin and carbonic anhydrase isoenzyme III (CAIII). Methods: Fifty-four laryngeal biopsy specimens from 18 LPR patients were studied by immunohistochemistry and Western blotting for pepsin, E-cadherin, and CAIII. These data were compared to those from normal control subjects analyzed in another research study. Results: Intracellular pepsin was detected in LPR patients, but not in controls. E-cadherin expression was reduced in patients with LPR. Carbonic anhydrase III expression was not found in the vocal fold or in the majority of samples taken from the ventricle of LPR patients and was inversely associated with E-cadherin membranous expression. Conclusions: The findings of depleted E-cadherin and CAIII and the presence of pepsin appear to correlate with LPR. The reduced protective response indicated by the reduced expression of CAIII may play an important role in the disruption of the intercellular barrier associated with the down-regulation of E-cadherin.
ISSN:0003-4894
1943-572X
DOI:10.1177/000348940511401204