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Cell biology of laryngeal epithelial defenses in health and disease: further studies. Ann Otol Rhinol Laryngol 2003 Jun;112(6):481-91

Date

07/02/2003

Pubmed ID

12834114

DOI

10.1177/000348940311200601

Scopus ID

2-s2.0-0038516590   138 Citations

Abstract

This is the second annual report of an international collaborative research group that is examining the cellular impact of laryngopharyngeal reflux (LPR) on laryngeal epithelium. The results of clinical and experimental studies are presented. Carbonic anhydrase (CA), E-cadherin, and MUC gene expression were analyzed in patients with LPR, in controls, and in an in vitro model. In patients with LPR, we found decreased levels of CAIII in vocal fold epithelium and increased levels in posterior commissure epithelium. The experimental studies confirm that laryngeal CAIII is depleted in response to reflux. Also, cell damage does occur well above pH 4.0. In addition, E-cadherin (transmembrane cell surface molecules, which have a key function in epithelial cell adhesion) was not present in 37% of the LPR laryngeal specimens. In conclusion, the laryngeal epithelium lacks defenses comparable to those in esophageal epithelium, and these differences may contribute to the increased susceptibility of laryngeal epithelium to reflux-related injury.

Author List

Johnston N, Bulmer D, Gill GA, Panetti M, Ross PE, Pearson JP, Pignatelli M, Axford SE, Dettmar PW, Koufman JA

Author

Nikki Johnston PhD Associate Professor in the Otolaryngology department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Acid-Base Equilibrium
Animals
Antibodies, Monoclonal
Biopsy
Blotting, Western
Cadherins
Carbonic Anhydrases
Epithelium
Esophagus
Gastroesophageal Reflux
Humans
Hydrogen-Ion Concentration
Immunohistochemistry
In Situ Hybridization
Laryngeal Diseases
Laryngeal Mucosa
Mucins
Swine
jenkins-FCD Prod-480 9a4deaf152b0b06dd18151814fff2e18f6c05280