Fatemeh Kiaee, Kiyana Bahani, Heshmat Shahi,
Volume 82, Issue 11 (February 2025)
Abstract
Background: Helicobacter pylori (H. pylori) infection is the most common infection worldwide and results in chronic gastritis, and rarely gastric carcinoma. Chronic inflammation, which is a major engine of disease development. Is dominantly controlled by adaptive and humoral immunity. This study reveals the intricate IL-21 and IL-23 relationship in H.pylori associated diseases as well as inflammatory GI disorders, as the crtically govern the differentiation and activity of T helper 17 (TH17) cells in the gastric mucosa. Understanding these cytokines pathways is essential for comprehending the immune pathogenesis of H. pylori infection and its outcome.
Methods: A literature search was conducted in the PubMed database using the MESH keywords "Helicobacter pylori" "Interleukin 21," "Interleukin 23," and "gastric cancer" to identify relevant English-language studies. Articles that were reviews, case reports, or letters to the editor were excluded.
Results: IL-23 significantly exacerbates both intestinal and gastric inflammatory responses by stimulating T cells particularly Th17 cell subsets, through the mediation of STAT3 signaling pathways and reducing IL-10 production, while T cells lacking the IL-23 receptor promote Treg expansion and intestinal homeostasis. IL-21 is implicated in chronic inflammation of the gastric and intestinal mucosa, with elevated levels observed in ulcerative colitis patients, contributing to the recruitment of inflammatory cells, increased inflammation, and angiogenesis. This particular cytokine plays an essential role in the recruitment of inflammatory cells, the increase of tissue inflammation, and the promotion of pathological angiogenesis. Moreover, IL-21 exerts influence over B cell differentiation and the production of antibodies, establishing a connection to humoral immune responses within chronic inflammations.
Conclusion: CD4+ T helper 17 (Th17) cells exhibit both antimicrobial and pathogenic immune functions in the gastrointestinal environment. These processes are interconnected, as cytokines such as IL-21 and IL-23 are essential for Th17 cell maintenance and support humoral immune responses. A comprehensive understanding of the dynamic immunological interactions in H. pylori-related and inflammatory gastrointestinal diseases may facilitate the development of novel immunology-based therapeutic interventions.
Heshmat Shahi , Fatemeh Kiaee ,
Volume 83, Issue 6 (September 2025)
Abstract
Helicobacter pylori is one of the most common chronic bacterial infections worldwide, with acquisition often occurring in childhood. While its role in the pathology of gastroduodenal diseases in adults is well-established, its impact on the pediatric population presents a unique set of clinical and pathophysiological challenges. This comprehensive review examines the complex and bidirectional relationship between Helicobacter pylori infection and host iron metabolism in pediatric and infant populations. For this review, the PubMed database was utilized for studies published from April 1979 through December 2024. Studies based on English language were included using the MESH terms "Helicobacter pylori," "iron," and "ferritin." According to the inclusion criteria, studies related to H. pylori infection and iron condition in patients under 18 years old were selected. Articles such as review articles, case reports, letters to the editor, and animal or in vitro studies were excluded. The main aim of this study was to illuminate the critical role of iron as an essential micronutrient and factor for both the host and the pathogen, examining the multifaceted mechanisms involved in H. pylori-induced iron homeostasis disruption in children.
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The findings indicate a multifaceted relationship: virulent Helicobacter pylori strains are significantly and inversely associated with true body iron stores, leading to Iron deficiency anemia (IDA). However, chronic inflammatory states can paradoxically elevate ferritin levels, masking underlying iron deficiency. Complex interaction between bacterial infection, host inflammatory responses, and iron deficiency is an important factor influencing both the severity of the damage caused by this bacterial infection and its chronicity in the pediatric population. Identification and comprehensive understanding of these complex mechanisms is of great importance for the effective management of iron deficiency anemia in children with H. pylori infection. Considering, increase in the incidence of H. pylori infection in childhood, it is essential that H. pylori infection be evaluation in children with unknown reasons IDA. Finally, screening methods for H. pylori infection in children is recommended, as this could improve long-term health outcomes.
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