Regulation of Ferroptosis by IL-33 Antibody in Asthma Exacerbations: Insights from Mouse Models

Interleukin-33 (IL-33) plays a critical role in asthma pathophysiology, particularly in exacerbations and airway inflammation. This study investigates the molecular mechanisms by which IL-33 modulates ferroptosis during asthma exacerbations. Through transcriptomic and proteomic analyses, IL-33 and GPX4 were identified as key factors in this process. In vitro experiments demonstrated that IL-33 antibody reduced inflammation and ferroptosis in IL-13-induced BEAS-2B cells, while in vivo validation in mice showed that the antibody decreased inflammatory responses, upregulated GPX4 expression, and improved asthma symptoms. These findings suggest that IL-33 antibody suppresses ferroptosis, alleviates inflammation, and modulates GPX4 expression, offering potential therapeutic targets for managing asthma exacerbations by modulating the IL-33 and ferroptosis pathways.