Erschienen in:
03.02.2024 | Original Research Paper
CCL18, CHI3L1, ANG2, IL-6 systemic levels are associated with the extent of lung damage and radiomic features in SARS-CoV-2 infection
verfasst von:
Ilaria Ferrigno, Laura Verzellesi, Marta Ottone, Martina Bonacini, Alessandro Rossi, Giulia Besutti, Efrem Bonelli, Rossana Colla, Nicola Facciolongo, Elisabetta Teopompi, Marco Massari, Pamela Mancuso, Anna Maria Ferrari, Pierpaolo Pattacini, Valeria Trojani, Marco Bertolini, Andrea Botti, Alessandro Zerbini, Paolo Giorgi Rossi, Mauro Iori, Carlo Salvarani, Stefania Croci
Erschienen in:
Inflammation Research
|
Ausgabe 4/2024
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Abstract
Objective and design
We aimed to identify cytokines whose concentrations are related to lung damage, radiomic features, and clinical outcomes in COVID-19 patients.
Material or subjects
Two hundred twenty-six patients with SARS-CoV-2 infection and chest computed tomography (CT) images were enrolled.
Methods
CCL18, CHI3L1/YKL-40, GAL3, ANG2, IP-10, IL-10, TNFα, IL-6, soluble gp130, soluble IL-6R were quantified in plasma samples using Luminex assays. The Mann–Whitney U test, the Kruskal–Wallis test, correlation and regression analyses were performed. Mediation analyses were used to investigate the possible causal relationships between cytokines, lung damage, and outcomes. AVIEW lung cancer screening software, pyradiomics, and XGBoost classifier were used for radiomic feature analyses.
Results
CCL18, CHI3L1, and ANG2 systemic levels mainly reflected the extent of lung injury. Increased levels of every cytokine, but particularly of IL-6, were associated with the three outcomes: hospitalization, mechanical ventilation, and death. Soluble IL-6R showed a slight protective effect on death. The effect of age on COVID-19 outcomes was partially mediated by cytokine levels, while CT scores considerably mediated the effect of cytokine levels on outcomes. Radiomic-feature-based models confirmed the association between lung imaging characteristics and CCL18 and CHI3L1.
Conclusion
Data suggest a causal link between cytokines (risk factor), lung damage (mediator), and COVID-19 outcomes.