Molecular and Functional Recovery of Esophageal Barrier Integrity After Laparoscopic Anti-reflux Surgery

Patients undergoing laparoscopic anti-reflux surgery (LARS) often experience improved quality of life and reduced gastroesophageal reflux disease (GERD) symptoms. This study aimed to assess the impact of LARS on epithelial remodeling and repair in the esophageal mucosa.

Upper gastrointestinal (GI) endoscopy was performed once on healthy controls (HC) and twice on GERD patients before and approximately 6 month after surgery, with esophageal biopsies collected. The expressions of E-cadherin (ECAD), Occludin (OCLN), Claudin 1 (CLDN1), Claudin 4 (CLDN4), Zonula Occludens -1 (ZO-1), and ZO-2 were analyzed in the biopsies, and dilated intercellular spaces (DIS) were examined under light microscopy.

The study included 22 GERD patients who were underwent for LARS, and 20 HCs. All patients had pathological reflux episodes. In the Post-LARS group, TEER increased significantly compared to Pre-LARS and HC (p < 0.05), while mucosal permeability decreased (p < 0.05). A significant negative correlation was found between TEER and permeability (p = 0.0002). DIS remained dilated in both Pre- and Post-LARS patients compared to HC (p < 0.05). Gene expression analysis revealed significant increases in ZO-1, OCLN, and ZO-2 Post-LARS (p < 0.05).

LARS improves mucosal integrity by enhancing TEER and reducing permeability in GERD patients, although DIS remains unchanged. The upregulation of tight junction genes such as ZO-1 and OCLN Post-LARS suggests that surgical intervention may support epithelial barrier restoration. DIS remains dilated after LARS; this might be reason that it is not an early marker in GERD pathogenesis. These findings enhance our understanding of GERD nature and may inform future target therapeutic strategies.