Akcin R, Saribas S, Kocazeybek B. Microbiota signatures and genetic risk in pediatric celiac disease. World J Gastroenterol 2026; 32(38): 119677 [DOI: 10.3748/wjg.119677]
Corresponding Author of This Article
Bekir Kocazeybek, Professor, Department of Medical Microbiology, Istanbul University-Cerrahpasa, Cerrahpasa Medical Faculty, Kocamustafapaşa St No. 53, İstanbul 34098, Türkiye. bzeybek@istanbul.edu.tr
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
review-article
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This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Gastroenterol. Oct 14, 2026; 32(38): 119677 Published online Oct 14, 2026. doi: 10.3748/wjg.119677
Microbiota signatures and genetic risk in pediatric celiac disease
Ruveyda Akcin, Suat Saribas, Bekir Kocazeybek
Ruveyda Akcin, Suat Saribas, Bekir Kocazeybek, Department of Medical Microbiology, Istanbul University-Cerrahpasa, Cerrahpasa Medical Faculty, İstanbul 34098, Türkiye
Ruveyda Akcin, Department of Medical Microbiology, Faculty of Medicine, Istanbul Health and Technology University, İstanbul 34320, Türkiye
Author contributions: Akcin R, Saribas S, and Kocazeybek B contributed to this paper; Kocazeybek B designed the overall concept; Akcin R contributed to the writing, discussion and design of the manuscript; Saribas S contributed to the editing the manuscript, illustrations, and review of literature. All authors have read and approved the final manuscript.
AI contribution statement: AI tools (Google Gemini) were used only for limited language assistance and editorial support, while the scientific content, interpretations, and intellectual framework of the manuscript were entirely developed by the authors.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Corresponding author: Bekir Kocazeybek, Professor, Department of Medical Microbiology, Istanbul University-Cerrahpasa, Cerrahpasa Medical Faculty, Kocamustafapaşa St No. 53, İstanbul 34098, Türkiye. bzeybek@istanbul.edu.tr
Received: February 3, 2026 Revised: April 22, 2026 Accepted: May 22, 2026 Published online: October 14, 2026 Processing time: 214 Days and 2.8 Hours
Abstract
Celiac disease (CD) is a chronic, immune-mediated enteropathy triggered by dietary gluten in genetically susceptible individuals, most commonly those carrying human leukocyte antigen-DQ2 or human leukocyte antigen-DQ8 haplotypes. However, because these haplotypes are prevalent in the general population while only a minority of carriers develop disease, additional factors are likely to contribute to disease onset and progression. In recent years, the gut microbiota has emerged as a potential mediator between host genetic susceptibility and environmental triggers, particularly in pediatric CD. Current evidence suggests that children with CD exhibit reduced microbial diversity, depletion of beneficial commensals, enrichment of proinflammatory taxa, and broader alterations extending to fungal and viral communities. However, these findings remain heterogeneous, largely due to variability in study design, sampling sites, diet, age, and analytical methods. This review examines the interplay between host genetic risk and the intestinal microbiota in pediatric CD, with emphasis on bacterial, fungal, and viral components. Moreover, it highlights the importance of longitudinal, functionally oriented, and multi-omics approaches, particularly in genetically at-risk yet clinically unaffected children, to better clarify causality and identify early microbial markers of disease susceptibility.
Core Tip: Pediatric celiac disease cannot be explained by host genetics alone. Although human leukocyte antigen-DQ2 and human leukocyte antigen-DQ8 are necessary risk factors in most patients, they do not fully account for disease onset or clinical heterogeneity. Current evidence suggests that the gut microbiota, including bacterial, fungal, and viral communities, may act as a dynamic interface between genetic predisposition and environmental exposures. Longitudinal and functional studies in at-risk children may help define early microbial signatures and improve future risk stratification.
