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Updated: Jan 22, 2026
DNBS/TNBS Colitis Models: Providing Insights Into Inflammatory Bowel Disease and Effects of Dietary Fat
Published on: February 27, 2014
Current concepts in pediatric inflammatory bowel disease; IL10/IL10R colitis as a model disease
Yousef Almana1, Reem Mohammed2
1Department of Pediatrics, Section of Pediatric Allergy and Immunology, King Faisal Specialist Hospital & Research Centre (KFSHRC), Riyadh, Saudi Arabia.
Insights
Genetic factors significantly influence pediatric inflammatory bowel disease (PIBD). This review details genetic mutations linked to very early-onset IBD (VEO-IBD), including IL10 and IL10 receptor defects.
Area of Science:
- Gastroenterology
- Immunology
- Genetics
Background:
- Inflammatory bowel disease (IBD) encompasses ulcerative colitis (UC) and Crohn's disease (CD).
- Pediatric IBD (PIBD) has strong genetic links, with rare, very early-onset IBD (VEO-IBD) identified in consanguineous populations.
- Understanding gut immunity, microbiome, immune dysregulation, and immunodeficiency is crucial.
Purpose of the Study:
- Review key players in gut immunity.
- Compare adult and pediatric IBD to explore monogenic vs. multifactorial disease relationships.
- List genetic mutations associated with VEO-IBD and summarize research on infantile colitis-related mutations (IL10/IL10 receptor).
Main Methods:
- Literature review of genetic factors in IBD.
- Comparative analysis of adult and pediatric IBD.
- Summary of genomic studies identifying VEO-IBD genetic defects.
Main Results:
- Genomic technologies have identified genetic defects in rare VEO-IBD.
- Specific genetic mutations are confirmed to be linked to VEO-IBD.
- Research has elucidated monogenic mutations, such as IL10 and IL10 receptor defects, in infantile colitis.
Conclusions:
- Genetic factors play a significant role in PIBD, particularly VEO-IBD.
- Investigating PIBD offers insights into monogenic and multifactorial diseases.
- Defects in IL10 and its receptor are implicated in infantile-onset IBD.
Abstract:
Inflammatory bowel disease (IBD) is a heterogeneous group of disorders composed mainly of ulcerative colitis (UC) and Crohn's disease (CD) and undetermined IBD. The peak incidence of occurrence is mainly beyond the pediatric age group. Recent knowledge about genetic factors had been strongly linked to pediatric IBD (PIBD). Recent advances in genomic technologies have prompted the identification of genetic defects underlying rare, very early-onset IBD (VEO-IBD) as a disease subgroup noted especially in populations with higher consanguinity rates. A better understanding of key players in the complex homeostasis of the immune system in the gut and illustrating the relationships between intestinal microbiome, systemic immune dysregulation and primary immunodeficiency have received growing recognition over the years. In this article, we provide a review of the key players of the immunity of the gut, compare between adult and pediatric IBD as an interesting module to investigate the relationship between monogenic and multifactorial/polygenic diseases, list genetic mutations confirmed to be linked to VEO IBD and summarize the scientific work that led to the discovery of one of the monogenic mutations related to infantile colitis, namely IL10 and IL10 receptor defects.
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