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논문 기본 정보

자료유형
학술저널
저자정보
Pelin Ergun (Departments of Medical Biochemistry, Faculty of Medicine, Ege University, Izmir, Turkey) Sezgi Kipcak (Department of Medical Biology, Faculty of Medicine, Ege University, Izmir, Turkey) Nur S Gunel (Department of Medical Biology, Faculty of Medicine, Ege University, Izmir, Turkey) Serhat Bor (Division of Gastroenterology, Faculty of Medicine, Ege University, Ege Reflux Study Group, Izmir, Turkey) Eser Y Sozmen (Departments of Medical Biochemistry, Ege University, Izmir, Turkey)
저널정보
대한소화관운동학회(현 대한소화기능성질환.운동학회) Journal of Neurogastroenterology and Motility (JNM) Journal of Neurogastroenterology and Motility (JNM) Vol.30 No.3
발행연도
2024.7
수록면
290 - 302 (13page)
DOI
10.5056/jnm22186

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Background/AimsGastroesophageal 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. MethodsPatients 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. ResultsThere 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. Conclusions“Microinflammation” in physiological acid exposure groups indicates 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.

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