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World J Gastrointest Endosc. May 16, 2026; 18(5): 119973
Published online May 16, 2026. doi: 10.4253/wjge.v18.i5.119973
Published online May 16, 2026. doi: 10.4253/wjge.v18.i5.119973
Letter to the Editor: Rethinking Helicobacter pylori-associated gastroduodenal disease through a systemic immune lens
Nebojsa Manojlovic, Clinic for Gastroenterology and Hepatology, Military Medical Academy, Medical Faculty of MMA, Belgrade 11000, Serbia
Stevan Manojlovic, Medical Faculty of Belgrade University, Belgrade 11000, Serbia
Author contributions: Manojlovic N designed the overall concept and outline of the manuscript; Manojlovic S contributed to the discussion and design of the manuscript; Manojlovic N and Manojlovic S contributed to the writing and editing of the manuscript, illustrations, and review of literature.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
AI contribution statement: AI tools were used for language polishing and translation.
Corresponding author: Nebojsa Manojlovic, MD, PhD, Full Professor, Clinic for Gastro
Received: February 24, 2026
Revised: March 10, 2026
Accepted: April 7, 2026
Published online: May 16, 2026
Processing time: 86 Days and 7.3 Hours
Revised: March 10, 2026
Accepted: April 7, 2026
Published online: May 16, 2026
Processing time: 86 Days and 7.3 Hours
Core Tip
Core Tip: Emerging evidence suggests that Helicobacter pylori-associated gastroduodenal diseases are shaped not only by local mucosal inflammation but also by stable, phenotype-specific systemic immune states. Recent findings indicate that bacterial eradication induces distinct systemic immune recalibration in gastritis and duodenal ulcer, particularly involving regulatory pathways such as interleukin-10 signaling. Recognizing this systemic immune dimension may refine the interpretation of immunological data and inform future research beyond a purely gastric framework.