Obesity-associated asthma is an increasingly prevalent and clinically challenging phenotype, characterized by poorer response to conventional asthma therapies, greater disease burden, and a distinct immunometabolic profile that sets it apart from classical eosinophilic asthma. Given the growing interest in therapies targeting the treatment of obesity, understanding the underlying biological mechanisms that drive inflammatory processes in this cohort is essential. Glucagon-like peptide-1 receptor agonists (GLP-1RAs) have emerged as transformative agents in the management of obesity and type 2 diabetes mellitus (T2DM), with a growing basis of evidence that their utility may extend beyond these indications and exert potent anti-inflammatory effects. In late 2025, the World Health Organization endorsed GLP-1RAs for obesity management, reframing how we contextualize care for patients living with obesity. In this review, we examine the immunopathological mechanisms underpinning obesity-associated asthma, and explore the biology of GLP-1 receptor signaling and the emerging preclinical and observational evidence supporting a direct role for GLP-1RAs in modulating pulmonary inflammation, airway remodeling, and immune cell activation. This could have important implications on future therapeutic directions. Key questions remain regarding whether any respiratory benefits are weight loss dependent or driven by direct immunomodulatory effects, and how GLP-1RAs should be positioned within treatment algorithms. Future prospective trials will be essential to define which patients derive the greatest benefit from these agents. GLP-1RAs represent a compelling and novel therapeutic avenue in obesity-associated asthma and potentially across the broader spectrum of chronic inflammatory airway disease.
