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已发表论文
IFI16、IL-33 和 CD55 的差异表达揭示了新冠肺炎和溃疡性结肠炎潜在的共同致病机制
Authors Zhang F, Di Q, Li Y, Ye J, Wang B, Ding Y
Received 28 May 2025
Accepted for publication 8 December 2025
Published 17 December 2025 Volume 2025:18 Pages 8027—8041
DOI https://doi.org/10.2147/JMDH.S543183
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Professor Charles V Pollack
Fang Zhang,1,2,* Quanzhao Di,3,* Yuanyuan Li,4,* Jianlan Ye,2 Bingcheng Wang,2 Yanbing Ding1
1Department of Gastroenterology, The Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, 225000, People’s Republic of China; 2Department of Outpatient, Jinling Hospital Affiliated to Nanjing University, Nanjing, 210000, People’s Republic of China; 3Endoscopy Center, Nanjing Traditional Chinese Medicine Hospital, Nanjing, 210000, People’s Republic of China; 4Department of Pharmacy, Eastern Theater Command Air Force Hospital, Nanjing, 210002, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Yanbing Ding, Email ybding@yzu.edu.cn Bingcheng Wang, Email 15063102@163.com
Background: The Coronavirus disease 2019 (COVID-19) pandemic has significantly impacted global health and shares several clinical features with ulcerative colitis (UC). However, the existence of a common pathological mechanism between COVID-19 and UC remains uncertain. Additionally, effective treatment strategies for UC patients infected with COVID-19 are not well established. In this study, we investigate the potential shared pathogenesis of UC and COVID-19 and explore possible therapeutic regimens through bioinformatics and systems biology approaches.
Methods: Common differentially expressed genes (DEGs) were extracted from the COVID-19 and ulcerative colitis (UC) datasets for functional enrichment, pathway analysis. The EnrichR database was used to predict potential transcription factors (TFs), microRNAs (miRNAs), and related drugs and diseases, enabling the construction of a regulatory network for both conditions.
Results: We identified 115 significant common DEGs, with 11 high-confidence hub genes—including IFI16, IL-33, and CD55—implicated in innate immunity and inflammatory regulation. Pathway analysis revealed enrichment in interferon signaling, neutrophil activation, and cytokine-mediated responses. Regulatory network reconstruction highlighted miR-155-5p and transcription factors (eg, STAT1) as key regulators. Drug repurposing efforts prioritized retinoic acid, cyclosporine, and TD-139, which target these shared mechanisms.
Conclusion: This study reveals robust molecular commonalities between COVID-19 and UC, highlighting dysregulated immune pathways and regulatory networks as shared mechanisms. We propose novel drug-repurposing candidates supported by network-based evidence, offering potential therapeutic strategies for patients with comorbid COVID-19 and UC.
Keywords: ulcerative colitis, COVID-19, GEO database, protein-protein interaction network, bioinformatics
1Department of Gastroenterology, The Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, 225000, People’s Republic of China; 2Department of Outpatient, Jinling Hospital Affiliated to Nanjing University, Nanjing, 210000, People’s Republic of China; 3Endoscopy Center, Nanjing Traditional Chinese Medicine Hospital, Nanjing, 210000, People’s Republic of China; 4Department of Pharmacy, Eastern Theater Command Air Force Hospital, Nanjing, 210002, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Yanbing Ding, Email ybding@yzu.edu.cn Bingcheng Wang, Email 15063102@163.com
Background: The Coronavirus disease 2019 (COVID-19) pandemic has significantly impacted global health and shares several clinical features with ulcerative colitis (UC). However, the existence of a common pathological mechanism between COVID-19 and UC remains uncertain. Additionally, effective treatment strategies for UC patients infected with COVID-19 are not well established. In this study, we investigate the potential shared pathogenesis of UC and COVID-19 and explore possible therapeutic regimens through bioinformatics and systems biology approaches.
Methods: Common differentially expressed genes (DEGs) were extracted from the COVID-19 and ulcerative colitis (UC) datasets for functional enrichment, pathway analysis. The EnrichR database was used to predict potential transcription factors (TFs), microRNAs (miRNAs), and related drugs and diseases, enabling the construction of a regulatory network for both conditions.
Results: We identified 115 significant common DEGs, with 11 high-confidence hub genes—including IFI16, IL-33, and CD55—implicated in innate immunity and inflammatory regulation. Pathway analysis revealed enrichment in interferon signaling, neutrophil activation, and cytokine-mediated responses. Regulatory network reconstruction highlighted miR-155-5p and transcription factors (eg, STAT1) as key regulators. Drug repurposing efforts prioritized retinoic acid, cyclosporine, and TD-139, which target these shared mechanisms.
Conclusion: This study reveals robust molecular commonalities between COVID-19 and UC, highlighting dysregulated immune pathways and regulatory networks as shared mechanisms. We propose novel drug-repurposing candidates supported by network-based evidence, offering potential therapeutic strategies for patients with comorbid COVID-19 and UC.
Keywords: ulcerative colitis, COVID-19, GEO database, protein-protein interaction network, bioinformatics