CXCL10 May Be Responsible for Susceptibility to Pulmonary Embolism in COVID-19 Patients

• Published in: Journal of inflammation research 2023-10, Vol.16, p.4913-4924
• Main Authors: Liu, Yingli, Si, Dan, Bai, Pingping, Zhu, Li, Zhang, Lili, Chen, Qi, Qi, Yong
• Format: Article
• Language: English
• Subjects: B cells; bioinformatics; coronavirus disease 2019; Coronaviruses; cxcl10; Epidermal growth factor; Genes; Original Research; Pulmonary embolism
• ISSN: 1178-7031; 1178-7031
• DOI: 10.2147/JIR.S431212

Although the potential of coronavirus disease 2019 (COVID-19) patients to develop pulmonary embolism (PE) is widely recognized, the underlying mechanism has not been completely elucidated. This study aimed to identify genes common to COVID-19 and PE to reveal the underlying pathogenesis of susceptibility to PE in COVID-19 patients. COVID-19 genes were obtained from the GEO database and the OMIM, CTD, GeneCards, and DisGeNET databases; PE genes were obtained from the OMIM, CTD, GeneCards, and DisGeNET databases. We overlapped the genes of COVID-19 and PE to obtain common genes for additional analysis, including functional enrichment, protein-protein interaction, and immune infiltration analysis. Hub genes were identified using cytoHubba, a plugin of Cytoscape, and validated using the independent datasets GSE167000 and GSE13535. The genes validated by the above datasets were further validated in clinical samples. We obtained 36 genes shared by PE and COVID-19. Functional enrichment and immune infiltration analyses revealed the involvement of cytokines and immune activation. Five genes (CCL2, CXCL10, ALB, EGF, and MKI67) were identified as hub genes common to COVID-19 and PE. CXCL10 was validated in both independent datasets (GSE167000 and GSE13535). Serum levels of CXCL10 in the COVID-19 group and the COVID-19 combined with PE group were significantly higher than those in the healthy control group (P