Abstract
Backgrounds Obesity has been recognised as a risk factor for poor asthma control. There is clinical evidence showing a poorer response to steroid therapy in obese asthmatic patients. However, the treatments to restore the poor corticosteroid sensitivity have not been established yet. Our objective was to establish a potential treatment for obese asthmatic patients.
Methods: Total 74 asthmatic patients (Obesity (OB), n= 52), Non-obesity (NOB) n=22) were recruited for this study. Peripheral blood mononuclear cells (PBMCs) were obtained and incubated with or without metformin and serial dilutions of dexamethasone for 1 hr, followed by stimulation with TNF-α. After overnight incubation, supernatants were harvested and CXCL8 in the supernatants was measured by ELISA. Then, IC50-Dex was calculated using the data.
Results: The IC50-Dex of PBMC obtained from the OB was significantly higher than that obtained from the NOB (p=0.002). The IC50-Dex of PBMC obtained from the OB significantly correlated with the number of acute exacerbations per year (ρ=0.310, p=0.028). In both groups, TNF-α-induced CXCL-8 releases were not affected by metformin treatments. In the OB, the metformin treatment significantly decreased the IC50-Dex of PBMC (p<0.001), but it did not in the NOB (p=0.926).
Conclusions: Metformin might be a drug candidate to restore poor corticosteroid sensitivity in obese asthmatic subjects.
Footnotes
Cite this article as Eur Respir J 2022; 60: Suppl. 66, 4344.
This article was presented at the 2022 ERS International Congress, in session “-”.
This is an ERS International Congress abstract. No full-text version is available. Further material to accompany this abstract may be available at www.ers-education.org (ERS member access only).
- Copyright ©the authors 2022
