# NLRP3 inflammasome expression in pediatric asthma: sputum-based insights, inflammatory mechanisms, and targeted therapeutic strategies

**Authors:** Mohammed AbuBaha, Samia Aldwaik, Bara Abubaha, Anwar Zahran, Dana Sandouka, Kareem Istetieh, Husam Hamshary, Mohammad Abushehadeh, Sarah Saife, Nadeen Sandoqah

PMC · DOI: 10.1186/s13223-025-01001-1 · Allergy, Asthma, and Clinical Immunology : Official Journal of the Canadian Society of Allergy and Clinical Immunology · 2025-11-29

## TL;DR

This paper reviews the role of the NLRP3 inflammasome in pediatric asthma, focusing on its involvement in inflammation and potential as a target for new treatments.

## Contribution

The paper highlights the potential of NLRP3 inflammasome as a novel therapeutic target for corticosteroid-resistant pediatric asthma.

## Key findings

- Elevated NLRP3 levels are associated with poor asthma control in children.
- NLRP3 inhibitors show potential in reducing airway inflammation in animal models.
- Current asthma treatments are less effective for neutrophilic or steroid-resistant asthma phenotypes.

## Abstract

Asthma is a common chronic inflammatory disease in children. Pediatric asthma has a wide range of immunologic phenotypes and different treatment responses. Recent data from various studies suggest that the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome, a cytosolic multiprotein complex, has a central role in innate immunity, may be implicated in pediatric asthma pathogenesis, especially in the neutrophilic corticosteroid-resistant type. This review article investigates the mechanism of NLRP3 inflammasome activation as well as its role in airway inflammation and its expression in pediatric asthma based on sputum studies. The findings emphasize an association between elevated NLRP3 levels and poor asthma control. The need for novel treatments is important because Current using therapies such as corticosteroids and biologics demonstrate variable efficacy. According to data, their efficacy heavily depends on the underlying inflammatory phenotype. Biologics such as mepolizumab, benralizumab, and dupilumab are well known for their corticosteroid-sparing effects especially in cases of severe eosinophilic asthma. even though, their therapeutic benefits are limited when it comes to neutrophilic or steroid-resistant phenotypes. NLRP3 inhibitors are new, promising treatments which emerged recently and show potential capability in reducing airway inflammation in animal models. Furthermore, NLRP3-driven inflammation appears to play a role not only in asthma but also in inflammatory bowel disease and juvenile idiopathic arthritis, indicating a wider relevance for therapies that target the inflammasome pathway. Although promising data, application of this data in clinical practice is still challenging due to many causes, including diagnostic challenges, ethical considerations in trials involving children, and the lack of approved NLRP3 inhibitors for use in children. More research is required and essential to confirm that NLRP3 could be used as a biomarker or therapeutic target in pediatric asthma.

## Linked entities

- **Genes:** NLRP3 (NLR family pyrin domain containing 3) [NCBI Gene 114548]
- **Diseases:** asthma (MONDO:0004979), inflammatory bowel disease (MONDO:0005265), juvenile idiopathic arthritis (MONDO:0011429)

## Full-text entities

- **Genes:** NLRP3 (NLR family pyrin domain containing 3) [NCBI Gene 114548] {aka AGTAVPRL, AII, AVP, C1orf7, CIAS1, CLR1.1}
- **Diseases:** airway inflammation (MESH:D007249), juvenile idiopathic arthritis (MESH:D001171), Asthma (MESH:D001249), inflammatory bowel disease (MESH:D015212)
- **Chemicals:** dupilumab (MESH:C582203), steroid (MESH:D013256), mepolizumab (MESH:C434107), benralizumab (MESH:C571386)

## Full text

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## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12771812/full.md

## References

6 references — full list in the complete paper: https://tomesphere.com/paper/PMC12771812/full.md

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Source: https://tomesphere.com/paper/PMC12771812