Laryngeal epithelial defenses against laryngopharyngeal reflux: investigations of E-cadherin, carbonic anhydrase isoenzyme III, and pepsin. Ann Otol Rhinol Laryngol 2005 Dec;114(12):913-21
Date
01/24/2006Pubmed ID
16425556DOI
10.1177/000348940511401204Scopus ID
2-s2.0-29744443713 76 CitationsAbstract
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.
Author List
Gill GA, Johnston N, Buda A, Pignatelli M, Pearson J, Dettmar PW, Koufman JAuthor
Nikki Johnston PhD Associate Professor in the Otolaryngology department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
BiopsyCadherins
Carbonic Anhydrase III
Epithelium
Gastroesophageal Reflux
Humans
Immunohistochemistry
Laryngeal Mucosa
Larynx
Pepsin A
Pharynx
