J Neurogastroenterol Motil  https://doi.org/10.5056/jnm22186
Roles of Cytokines in Pathological and Physiological Gastroesophageal Reflux Exposure
Pelin Ergun,1,3* Sezgi Kipcak,2,3 Nur S Gunel,2 Serhat Bor,3 and Eser Y Sozmen1
Departments of 1Medical Biochemistry, 2Medical Biology, Faculty of Medicine, Ege University, Izmir, Turkey; and 3Division of Gastroenterology, Faculty of Medicine, Ege University, Ege Reflux Study Group, Izmir, Turkey
Correspondence to: Pelin Ergun, PhD
Department of Medical Biochemistry, Faculty of Medicine, Ege University, 35100 Bornova, Izmir, Turkey
Tel: +90-232-390-5231, E-mail: pelinergun@yahoo.com, pelin.ergun@ege.edu.tr
Received: November 4, 2022; Revised: January 29, 2023; Accepted: April 10, 2023; Published online: November 14, 2023
© The Korean Society of Neurogastroenterology and Motility. All rights reserved.

Gastroesophageal reflux disease is frequently observed and has no definitive treatment. There are 2 main views on the pathogenesis of gastroesophageal reflux disease. The first is that epithelial damage starts from the mucosa by acidic-peptic damage and the inflammatory response of granulocytes. The other view is that T-lymphocytes attract chemoattractants from the basal layer to the mucosa, and granulocytes do not migrate until damage occurs. We aim to investigate the inflammatory processes occurring in the esophageal epithelium of the phenotypes at the molecular level. We also examined the effects of these changes on tissue integrity.
Patients with mild and severe erosive reflux, nonerosive reflux, reflux hypersensitivity, and functional heartburn were included. Inflammatory gene expressions (JAK/STAT Signaling and NFKappaB Primer Libraries), chemokine protein levels, and tissue integrity were examined in the esophageal biopsies.
There was chronic inflammation in the severe erosion group, the acute response was also triggered. In the mild erosion group, these 2 processes worked together, but homeostatic cytokines were also secreted. In nonerosive groups, T-lymphocytes were more dominant. In addition, the inflammatory response was highly triggered in the reflux hypersensitivity and functional heartburn groups, and it was associated with physiological reflux exposure and sensitivity.
“Microinflammation” in physiological acid exposure groups indicate that even a mild trigger is sufficient for the initiation and progression of inflammatory activity. Additionally, the anti-inflammatory cytokines were highly increased. The results may have a potential role in the treatment of heartburn symptoms and healing of the mucosa.
Keywords: Cytokines; Esophagus; Gastroesophageal reflux; Inflammation

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