Targeting IL-33 to suppress ferroptosis and alleviate inflammation in asthma exacerbations

In the context of asthma pathophysiology, especially during exacerbations and airway inflammation, interleukin-33 (IL-33) holds a pivotal role. This study delves into elucidating the impact of IL-33 on Ferroptosis during asthma exacerbations. Through comprehensive transcriptomic and proteomic analyses, IL-33 and GPX4 emerged as crucial regulators in this intricate process. In vitro experiments showcased the remarkable anti-inflammatory and ferroptosis-mitigating effects of an IL-33 antibody in IL-13-induced BEAS-2B cells. Subsequent in vivo validation in mice underscored the ability of the IL-33 antibody to diminish inflammatory responses, enhance GPX4 expression, and ameliorate asthma symptoms. These compelling findings suggest that the IL-33 antibody holds promise in suppressing Ferroptosis, alleviating inflammation, and modulating GPX4 expression, thereby proposing novel therapeutic strategies for managing asthma exacerbations by targeting the IL-33 and Ferroptosis pathways.

Airway inflammation response; Allergic asthma; Ferroptosis; GPX4; IL-33; Inflammation; Therapeutic targets.