Microbiota signatures and genetic risk in pediatric celiac disease

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Küçük Resim

Tarih

2026

Dergi Başlığı

Dergi ISSN

Cilt Başlığı

Yayıncı

Baishideng Publishing Group Inc.

Erişim Hakkı

info:eu-repo/semantics/openAccess

Araştırma projeleri

Organizasyon Birimleri

Dergi sayısı

Özet

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 hap lotypes. 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 suscept ibility 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 alte rations extending to fungal and viral communities. However, these findings re main 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.

Açıklama

Anahtar Kelimeler

Gut Microbiota, Human Leukocyte Antigen, Mycobiome, Pediatric Celiac Disease, Virome

Kaynak

World Journal of Gastroenterology

WoS Q Değeri

Q1

Scopus Q Değeri

Q1

Cilt

32

Sayı

38

Künye

Akçin, R., Sarıbaş, S., & Kocazeybek, B. (2026). Microbiota signatures and genetic risk in pediatric celiac disease. World Journal of Gastroenterology, 32(38), pp. 1-12. https://dx.doi.org/10.3748/wjg.119677