IL-8, TNF-α, and IL-17 in the Development of Erosive Esophagitis and Symptom Perception in Gastroesophageal Reflux Disease (GERD).

The diverse clinical characteristics of erosive esophagitis (EE) and symptom perception in patients with gastroesophageal reflux disease (GERD) remain a major challenge in understanding their underlying pathogenesis. This study aimed to investigate the association between the levels of IL-8, TNF-α, and IL-17 in serum and the presence of erosive esophagitis and symptoms related to GERD. We enrolled 65 subjects presenting with GERD symptoms. Based on the findings of upper endoscopy, the subjects were categorized into two groups: (1) erosive esophagitis (EE LA grades B-D) and (2) non-erosive esophagitis (normal-EE LA grade A). Symptom perception was assessed via GERD questionnaire (GERD-Q) and the frequency scale for the symptoms of GERD (FSSG). The enzyme-linked immunosorbent assay (ELISA) method was used to analyze serum levels of IL-8, TNF-α, and IL-17. Analysis of cytokine levels between different symptoms severity was performed using the Kruskal-Wallis H test. Median serum IL-8 levels were significantly higher in the erosive esophagitis group compared to those with non-erosive esophagitis (20.2 (IQR 16.9-32.2) vs. 17.7 (IQR 15.2-19.6), < 0.05). The study found a significant association between IL-8 levels and the presence of globus symptoms (median IL8 level 46.961 (38.622-92.644) in subjects with globus vs. 18.06 (16.68-20.49) in those without globus; < 0.05). Similarly, TNF-α levels were associated with the frequency of regurgitation symptoms (H index = 10.748; dr = 3; < 0.05). We observed a significant correlation between IL-17 levels and the frequency of heartburn and early satiety symptoms. IL-8 may play a role in the development of mucosal erosion in GERD. IL-8, TNF- α, and IL-17 might be involved in the development of globus symptoms, the frequency of regurgitation, and the frequency of heartburn and early satiety, respectively. The diverse symptom phenotypes observed in patients with GERD symptoms may be mediated by distinct profiles of proinflammatory cytokines.