Cell biology of laryngeal epithelial defenses in health and disease: further studies. Ann Otol Rhinol Laryngol 2003 Jun;112(6):481-91
Date
07/02/2003Pubmed ID
12834114DOI
10.1177/000348940311200601Scopus ID
2-s2.0-0038516590 (requires institutional sign-in at Scopus site) 174 CitationsAbstract
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 JAAuthor
Nikki Johnston PhD Professor in the Otolaryngology department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
Acid-Base EquilibriumAnimals
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
