Asthma is a chronic airway disease characterized by exacerbated inflammation, hyperresponsiveness, and associated bronchial remodeling. Despite innovative biotherapies, severe asthma remains largely uncontrolled, highlighting the need for new therapeutic approaches. Rac1 GTPase has recently been identified as a major contributor to bronchial hyperresponsiveness and remodeling. In this study, we demonstrate Rac1 overactivation in pulmonary eosinophils of asthmatic patients. Identifying the role of Rac1 GTPase in the molecular mechanisms of polymorphonuclear cells during allergic asthma could validate Rac1 as an innovative therapeutic target for severe asthma.
Keywords: Asthme sévère; Degranulation; Dégranulation; Eosinophils; Inflammation pulmonaire; Pulmonary inflammation; Rac1; Severe asthma; Éosinophile.
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