Send to

Choose Destination
Otolaryngol Head Neck Surg. 2005 Nov;133(5):718-24.

Proton pump (H+/K+-ATPase) expression in human laryngeal seromucinous glands.

Author information

Department of Otolaryngology-Head and Neck Surgery, Mount Sinai School of Medicine, New York, NY 10029, USA.



Recent pilot research suggested that the H+/K+-ATPase (proton pump), which is the target of pharmacotherapy for laryngopharyngeal reflux disease (LPRD), is associated with human laryngeal submucosal glands. The hypothesis of this study is that proton pump is expressed in the human larynx, and is not solely associated with the parietal cells of the stomach.


Fifteen surgical larynx subjects (27 pathologic specimens) containing seromucinous glands from banked tissue were retrospectively obtained after approval from Human Subjects Committee. Banked human stomach tissue was also obtained for comparative positive and negative controls. Sections were immunostained with two monoclonal antibodies selectively reactive with alpha or beta subunits of the H+/K+-ATPase (proton) pump.


In the human larynx, positive staining was seen in 14 of 15 subjects. Twenty-six specimens showed consistent staining in the seromucinous cells and ducts for the alpha subunit, and 23 specimens for the beta subunit. Stomach parietal cells exhibited strongly positive staining for both the alpha and beta subunits of the proton pump. There was no staining in stomach cells that were not morphologically consistent with the parietal cell.


The H+/K+-ATPase (proton) pump is present in seromucinous cells and ducts in the human larynx, with some variable expression noted. Proton pump involvement in human laryngeal seromucinous glands may explain heightened laryngeal sensitivity in those patients with chronic laryngitis believed to have LPRD. Also, proton pump inhibitor pharmacotherapy may have a site of action in the human larynx, explaining some of the controversies attributable to LPRD.



[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Atypon
Loading ...
Support Center