Allergic Inflammation and the IL-33/ST2 Axis in Childhood Asthma: A Narrative Review of Related Pathways and Intervention Strategies.

Background

Pediatric asthma is the most common disease in children, and its incidence is increasing globally. Its clinical features are usually wheezing, dyspnea, cough, and increased airway sensitivity. Exposure to dust mites in the living environment, air pollutants, and virus infections can lead to asthma. Currently, the main clinical treatment options include environmental interventions, glucocorticoids, anti-allergy drugs, and biologics targeting type-2 inflammation. However, challenges remain due to the complexity of the etiology and pathobiology of pediatric asthma.

Results

Interleukin-33 (IL-33) is an important member of the IL-1 cytokine family, which is produced mainly by epithelial cells and endothelial cells and binds to the receptor ST2. In inflammatory responses, IL-33/ST2 mediates the activation and recruitment of immune cells, including Th2 cells, mast cells, and eosinophils. Recent studies have revealed that IL-33/ST2 plays a crucial role in allergic asthma. This review systematically summarizes the changes in the expression of the IL-33/ST2 signaling axis and its core pathogenic mechanisms during the occurrence and development of allergic asthma. Moreover, we summarize the current clinical intervention strategies for childhood allergic asthma, aiming to provide new insights for the treatment of this disease.