Abstract
In the absence of visible mucosal damage, it is hypothesized that the esophageal mucosal barrier is functionally impaired in patients with non-erosive reflux disease (NERD). The aim of the present study was to perform an exploratory analysis of the mucosal barrier in NERD compared to erosive esophagitis (EE) and controls. A second aim was to explore TRPV1 gene transcription in relation to the mucosal barrier function and heartburn symptoms. In this prospective study, 10 NERD patients, 11 patients with active erosive esophagitis and 10 healthy volunteers were included. Biopsies from non-eroded mucosa were obtained for (1) ex vivo analyses (Ussing chamber) of transepithelial electrical resistance (TEER) and permeability (2) gene transcription of tight-junction proteins and transient receptor potential vanilloid subfamily member 1 (TRPV1). No differences in TEER or permeability were found between NERD and healthy volunteers, whereas TEER was lower in patients with erosive esophagitis. TRPV1 gene transcription was not significantly different between EE, NERD and controls. Conclusions: esophageal mucosal barrier function and TRPV1 transcription is not significantly altered in NERD patients. Future research is needed to explore other potential mechanisms that may account for the high symptom burden in these patients.
Highlights
In health, the multilayer of the squamous epithelium of the esophageal mucosa serves as a barrier and prevents contact of refluxed luminal content with nociceptive afferents and subsequent excitation, leading to heartburn
A total of 22 patients with gastroesophageal reflux disease (GERD) and 12 healthy volunteers were included in the study
One patient who was not able to stop acid suppressive therapy and two healthy volunteers with esophagitis were excluded at endoscopy in absence of any symptoms
Summary
The multilayer of the squamous epithelium of the esophageal mucosa serves as a barrier and prevents contact of refluxed luminal content with nociceptive afferents and subsequent excitation, leading to heartburn. In patients with erosive esophagitis (EE), the barrier function is visibly impaired and reflux can reach the exposed afferents. In patients with non-erosive reflux disease (NERD), the esophageal mucosa appears normal on endoscopy and the mechanisms leading to heartburn are less clear. Previous studies postulated that the histological finding of dilated intercellular spaces (DIS) in the basal and prickle cell layers of the mucosa of NERD patients is the manifestation of a mucosal barrier defect [4,5]. A more elegant and validated method to study the functionality of the mucosal barrier ex vivo is to use the Ussing chamber technique [8]
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