Published online Mar 16, 2026. doi: 10.4253/wjge.v18.i3.116958
Revised: January 7, 2026
Accepted: January 21, 2026
Published online: March 16, 2026
Processing time: 108 Days and 9.3 Hours
Although Helicobacter pylori (H. pylori) infection is widely known to induce chronic gastric inflammation, its contribution to low-grade sustained systemic inflammation remains unclear.
To investigate the effect of H. pylori eradication on systemic inflammatory activity through the analysis of serum cytokine levels in patients with either gastritis (GA) or duodenal ulcer (DU).
We included fifty-four patients who underwent upper gastrointestinal endoscopy for dyspepsia and were diagnosed with either H. pylori-positive GA or DU. Serum cytokine levels were measured before and after bacterial eradication using enzyme-linked immunosorbent assay. Paired comparisons within each group (GA and DU) were performed using Wilcoxon signed-rank test. Differences between groups at baseline and post-treatment were analyzed using Mann-Whitney U test. To account for multiple testing across cytokines, P values were adjusted using the false discovery rate approach according to the Benjamini-Hochberg procedure.
In the GA group, all measured cytokines: Interleukin (IL)-1α, IL-1β, IL-2, IL-6, IL-8, IL-10, IL-12p70, IL-23, interferon gamma (IFN-γ), and tumor necrosis factor-alpha (TNF-α)-showed significant post-treatment reductions. In the DU group, most cytokines decreased, but IL-2 and IL-12p70 did not reach sta
Our findings suggest that H. pylori eradication is associated with reduced pro-inflammatory cytokine levels in patients with GA and with a distinct shift toward an anti-inflammatory profile in patients with DU, highlighting a broader systemic immunological context beyond the gastric niche.
Core Tip: Helicobacter pylori (H. pylori) infection is consistently associated with chronic gastric inflammation and may also relate to sustained low-grade systemic inflammatory activity. In this study, distinct circulating cytokine patterns were observed in patients with gastritis (GA) and duodenal ulcer (DU) following bacterial eradication, with attenuation of pro-inflammatory mediators in GA and a regulatory-skewed cytokine profile in DU. These findings highlight a potential systemic immunological dimension of H. pylori-associated disease, with relevance for inflammation-related conditions beyond the gastric compartment.
