Pediatric Severe Asthma Management and Pathophysiology
Summary
Pediatric severe asthma is characterised by persistent symptoms and frequent exacerbations despite high-dose inhaled therapies. Management strategies emphasise precision medicine, combining pharmacological step-up—such as increasing inhaled corticosteroid dose or adding long-acting β₂-agonists—with biologic agents targeting type 2 inflammatory pathways. Advances in clinical phenotyping and non-invasive biomarkers have refined the identification of eosinophilic, neutrophilic and paucigranular subtypes, guiding tailored interventions. Pathophysiologically, severe asthma in children involves dysregulated airway remodelling, including smooth muscle hypertrophy, subepithelial fibrosis and aberrant microvascular changes. Innate immune cells—particularly type 2 innate lymphoid cells and Th2 lymphocytes—drive eosinophilic inflammation, while mast cell mediators contribute to airway hyperresponsiveness. Environmental factors, such as allergen exposures and passive smoke, exacerbate oxidative stress and impair corticosteroid responsiveness. A multidisciplinary approach that integrates biomarker-guided therapy, environmental control and ongoing functional assessment optimises long-term lung growth and minimises morbidity.
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Pediatric Severe Asthma Management and Pathophysiology publication trend
The graph below shows the total number of articles in pediatric severe asthma management and pathophysiology across all publications each year (not limited to Nature Index journals).
Technical terms
Inhaled corticosteroids (ICS): Anti-inflammatory medications delivered by inhalation to reduce airway eosinophilia and swelling.
Long-acting β₂-agonists (LABA): Bronchodilators that relax airway smooth muscle over an extended period to improve airflow.
Type 2 innate lymphoid cells (ILC2s): Innate immune cells that produce type 2 cytokines (IL-5, IL-13) and contribute to eosinophilic inflammation.
Pericytes: Perivascular cells that support capillary stability and regulate angiogenesis in the airway microvasculature.
Mast cells: Tissue-resident immune cells that release proteases and mediators triggering bronchoconstriction and vascular leakage.
Airway hyperresponsiveness (AHR): Exaggerated airway narrowing in response to stimuli, characteristic of asthma severity.
References
- Best step-up treatments for children with uncontrolled asthma: a systematic review and network meta-analysis of individual participant data. European Respiratory Journal (2023).
- Mast cell activation disrupts interactions between endothelial cells and pericytes during early life allergic asthma. Journal of Clinical Investigation (2024).
- Location, Location, Location: Spatial Immune‐Stroma Crosstalk Drives Pathogenesis in Asthma. Immunological Reviews (2025).
- Pathophysiological Mechanisms of Asthma. Frontiers in Pediatrics (2019).
- Passive Smoking Impairs Histone Deacetylase-2 in Children With Severe Asthma. CHEST Journal (2013).
- Pulmonary type-2 innate lymphoid cells in paediatric severe asthma: phenotype and response to steroids. European Respiratory Journal (2019).
- Pericytes contribute to airway remodeling in a mouse model of chronic allergic asthma. American Journal of Physiology - Lung Cellular and Molecular Physiology (2015).
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