# Role of NLRP3 Inflammasomes in Disorders of Children’s Digestive Systems: A Narrative Review

**Authors:** Safaa ELMeneza

PMC · DOI: 10.3390/pediatric17050103 · Pediatric Reports · 2025-10-07

## TL;DR

This review explores how NLRP3 inflammasomes influence digestive and liver disorders in children, highlighting their dual role in both protecting and causing disease.

## Contribution

The paper provides a focused narrative review on NLRP3 inflammasomes in pediatric gastrointestinal and hepatic disorders, identifying potential therapeutic applications.

## Key findings

- NLRP3 inflammasomes are involved in both protecting and causing gastrointestinal and hepatic diseases in children.
- Few studies specifically address NLRP3's role in pediatric conditions like autism, IBD, and autoimmune diseases.
- Pharmacological inhibitors of NLRP3 inflammasomes may offer future therapies for pediatric gastrointestinal issues.

## Abstract

Background/Objectives: This review article highlights the role of the nucleotide-binding domain, leucine-rich repeat, pyrin domain-containing 3 protein (NLRP3) inflammasomes in various gastrointestinal and hepatic disorders in the pediatric age group. NLRP3 inflammasomes are one of the principal intracellular innate immune sensors. During inflammation, molecules such as caspase-1 and the release of IL-1β and IL-18 are produced. The NLRP3 inflammasome participates in the preservation of intestinal homeostasis and mucosal immune response. The objective is to evaluate the published articles related to the role of NLRP3 inflammasomes in common pediatric gastrointestinal and hepatic disorders in order to identify the future perspective regarding their possible therapeutic values. Methods: We searched Medline for NLRP3 inflammasomes and disorders of the digestive system during childhood. Results: Although the majority of articles were related to various disorders of adults, such as Alzheimer’s disease, Parkinson’s disease, atherosclerosis, as well as neurodevelopmental disorders, such as schizophrenia, a few published datasets were related to the roles of NLRP3 in the pediatric age group: they addressed autism, rheumatoid arthritis, and other autoimmune diseases, as well as inflammatory bowel diseases (IBD) and hepatic infection. Some research demonstrated that the NLRP3 inflammasome has a protective role; however, it also has a pathogenic function. Conclusions: This review focused on the comprehensive role of inflammasome NLRP3 in the most common pediatric and neonatal gastrointestinal and hepatic diseases, including clinical and experimental studies, as well as the pharmacological inhibitors for NLRP3 inflammasomes, which may provide future therapy for GIT problems, such as IBD.

## Linked entities

- **Genes:** NLRP3 (NLR family pyrin domain containing 3) [NCBI Gene 114548]
- **Proteins:** NLRP3 (NLR family pyrin domain containing 3), Caspase1 (caspase-1), IL1B (interleukin 1 beta), IL18 (interleukin 18)
- **Diseases:** autism (MONDO:0005260), rheumatoid arthritis (MONDO:0008383)

## Full-text entities

- **Genes:** IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, NLRP3 (NLR family pyrin domain containing 3) [NCBI Gene 114548] {aka AGTAVPRL, AII, AVP, C1orf7, CIAS1, CLR1.1}, CASP1 (caspase 1) [NCBI Gene 834] {aka ICE, IL1BC, P45}, IL18 (interleukin 18) [NCBI Gene 3606] {aka IGIF, IL-18, IL-1g, IL1F4}
- **Diseases:** hepatic infection (MESH:D056486), autoimmune diseases (MESH:D001327), gastrointestinal and hepatic diseases (MESH:D005767), IBD (MESH:D015212), schizophrenia (MESH:D012559), inflammation (MESH:D007249), rheumatoid arthritis (MESH:D001172), Parkinson's disease (MESH:D010300), atherosclerosis (MESH:D050197), autism (MESH:D001321), neurodevelopmental disorders (MESH:D002658), Alzheimer's disease (MESH:D000544), disorders of the digestive system (MESH:D004066)

## Full text

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## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC12566619/full.md

## References

90 references — full list in the complete paper: https://tomesphere.com/paper/PMC12566619/full.md

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Source: https://tomesphere.com/paper/PMC12566619