[Background] In adult asthma, obesity-related non-eosinophilic asthma has been identified as a phenotype of asthma, which is characterized by late-onset, female predominance, and an increased frequency of severe symptoms. In addition to the phenotype, we identified a phenotype of obese asthma characterized by type 2 inflammation dominant, lower lung function, and more likely with acute exacerbation (Masako To et.al. ERJ 2020; 56: Suppl. 64, 192.). However, the influence of adipocytokines in the phenotype is not clarified yet. This study aimed to investigate the difference in adipocytokines and cytokines profiles between obese asthmatic patients with type 2 inflammation dominant and those with non-type 2 inflammation dominant.

[Methods] Adult obese asthmatic patients were recruited for this study. The patients were classified into two groups: those with positive type 2 inflammation markers (eosinophil counts?300/?L and/or a specific allergen is detected, T2) and those with negative non-type 2 inflammation markers (NT2). Clinical parameters and serum cytokine levels were compared between the groups.

[Results] A total of 57 (38 in T2 and 19 in NT2) obese patients with asthma were recruited. Serum eosinophil counts and IgE levels in T2 were significantly higher than those in NT2. Serum leptin, PAI-1, and IL-6 levels did not differ between T2 and NT2. No significant difference was detected in the serum oxidative stress marker, 8-OHdG, levels between the groups.

 [Conclusions] Obesity-related non-type 2 inflammation as well as type 2 inflammation is involved in the pathogenesis of obese asthma in T2. The overlapped inflammation may induce severer asthma in the phenotype.