The Role of Obesity-Related Chronic Inflammation in the Pathogenesis and Severity of Asthma in Adults: A Systematic Review

Obesity and asthma are common chronic conditions that frequently coexist in adults and contribute to a substantial clinical and public health burden. Although excess body weight affects asthma through mechanical effects on lung volumes and airway closure, current evidence increasingly supports the role of obesity-related chronic low-grade inflammation as a central mechanism linking obesity with asthma development, severity, symptom burden, exacerbation risk, and therapeutic response. This systematic review summarizes contemporary evidence on the role of adipose-tissue inflammation, adipokines, cytokine signaling, metabolic dysfunction, oxidative stress, and immune dysregulation in the pathogenesis and clinical expression of obesity-related asthma in adults. A structured literature search was performed using major biomedical databases, with priority given to systematic reviews, meta-analyses, clinical reviews, cohort studies, mechanistic studies, and current asthma guidelines. The available literature indicates that obesity-related asthma is not a single uniform phenotype but a heterogeneous clinical entity involving overlapping inflammatory, metabolic, mechanical, and behavioral pathways. Increased systemic inflammatory activity, altered leptin and adiponectin signaling, elevated interleukin-6, neutrophilic airway inflammation, insulin resistance, and comorbidities such as obstructive sleep apnea and gastroesophageal reflux may all contribute to worse asthma control. Clinical management should therefore extend beyond inhaled pharmacotherapy and include assessment of obesity as a treatable trait, weight management, comorbidity screening, lifestyle intervention, and individualized evaluation of inflammatory phenotype. Future studies should clarify causal mechanisms and determine which interventions most effectively improve asthma outcomes in adults with obesity.