Lysophospholipid metabolism, clinical characteristics, and artificial intelligence-based quantitative assessments of chest CT in patients with stable COPD and healthy smokers.
Authors
Affiliations (4)
Affiliations (4)
- Department of Respiratory and Critical Care Medicine, Peking University Third Hospital, Beijing, 100191, People's Republic of China.
- Department of Respiratory and Critical Care Medicine, Tibet Autonomous Region People's Hospital, Lhasa, 850000, People's Republic of China.
- Yizhiyuan Health Technology (Hangzhou) Co., Ltd.,, Hangzhou, 311121, People's Republic of China.
- Department of Respiratory and Critical Care Medicine, Peking University Third Hospital, Beijing, 100191, People's Republic of China. [email protected].
Abstract
The specific role of lysophospholipids (LysoPLs) in the pathogenesis of chronic obstructive pulmonary disease (COPD) is not yet fully understood. We determined serum LysoPLs in 20 patients with stable COPD and 20 healthy smokers using liquid chromatography-mass spectrometry (LC-MS) and matching with the lipidIMMS library, and integrated these data with spirometry, systemic inflammation markers, and quantitative chest CT generated by an automated 3D-U-Net artificial intelligence algorithm model. Our findings identified three differential LysoPLs, lysophosphatidylcholine (LPC) (18:0), LPC (18:1), and LPC (18:2), which were significantly lower in the COPD group than in healthy smokers. Significant negative correlations were observed between these LPCs and the inflammatory markers C-reactive protein and Interleukin-6. LPC (18:0) and (18:2) correlated with higher post-bronchodilator FEV1, and the latter also correlated with FEV1% predicted, forced vital capacity (FVC), and FEV1/FVC ratio. Additionally, these three LPCs were negatively correlated with the volume and percentage of low attenuation areas (LAA), high-attenuation areas (HAA), honeycombing, reticular patterns, ground-glass opacities (GGO), and consolidation on CT imaging. In the patients with COPD, the three LPCs were most significantly associated with HAA and GGO. In conclusion, patients with stable COPD exhibited a unique LysoPL metabolism profile, with LPC (18:0), LPC (18:1), and LPC (18:2) being the most significantly altered lipid molecules. The reduction in these three LPCs was associated with impaired pulmonary function and were also linked to a greater extent of emphysema and interstitial lung abnormalities.