Related Experiment Video
Updated: May 12, 2026

Real-Time, Semi-Automated Fluorescent Measurement of the Airway Surface Liquid pH of Primary Human Airway Epithelial Cells
Published on: June 13, 2019
Human esophageal secretion: mucosal response to luminal acid and pepsin
Z Namiot1, J Sarosiek, R M Rourk
1University of Virginia Health Sciences Center, Charlottesville.
Background/Aims:
Although esophageal histology in humans reveals numerous submucosal mucous glands, their secretion has never been explored. Therefore, we have studied the chemical composition and physical characteristics of esophageal secretion under the impact of luminal saline, acid, and acid/pepsin solutions.
Methods:
The esophageal lumen in 21 healthy volunteers was continuously perfused with saline, HCI, or HCI/pepsin. Perfusates were assayed for mucin, protein, and viscosity. In addition, analysis of amino acid and sugar composition of purified esophageal mucin was performed.
Results:
Esophageal perfusion with saline resulted in luminal release of mucin at the rate of 0.23 +/- 0.03 mg.cm-2 x min-1. Acid/pepsin solution significantly enhanced luminal release of mucin (0.32 +/- 0.03 mg.cm-2 x min-1; P < 0.01). HCI/pepsin solution also significantly increased the luminal output of protein (P < 0.01) and significantly impaired the viscosity of the esophageal perfusate (P < 0.05). Threonine, serine, and proline were the major amino acids within the esophageal mucin, whereas galactose was the predominant carbohydrate.
Conclusions:
Luminally released esophageal mucin, shown for the first time in humans, contributes significantly to maintaining the high viscosity of esophageal secretions. Significant increase in the luminal release of mucin under the impact of acid and pepsin, with subsequent decline of the perfusate viscosity, may indicate that mucin is the major target for gastric acid and pepsin, absorbing the deleterious impact of the gastroesophageal refluxate.
Related Concept Videos
Stomach pH Regulation
The acid-secreting gastric mucosal epithelial cells (parietal cells) lining the stomach lumen maintain the low pH in the lumen. Numerous ion transporters and channels on these parietal...
Pathophysiology of Peptic Ulcer Disease: Injurious Factors
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds to M3...
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors
Gastric Phase of Digestion
When food enters the stomach, it stretches the stomach walls and activates stretch receptors. This triggers local reflexes of the enteric nervous system, mediated through the myenteric plexus. These...
Mucosal Barrier of the Stomach
Within parietal cells, carbonic acid is first formed through the reaction of water and carbon dioxide. The dissociation of carbonic acid releases bicarbonate and hydrogen ions. The bicarbonate...
Peptic Ulcer Disease II: Pathophysiology
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.

