Bioinformatic analyses hinted at augmented T helper 17 cell differentiation and cytokine response as the central mechanism of COVID-19-associated Guillain-Barre syndrome
单位：[1]Department of Orthopaedic Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China[2]CUHK-Shenzhen Research Institute, Shenzhen, China[3]Department of Orthopedic Surgery, Beijing Jishuitan Hospital, Fourth Clinical College of Peking University, Jishuitan Orthopaedic College of Tsinghua University, Beijing, China[4]Department of Orthopaedic Surgery, Center for Osteonecrosis and Joint Preserving & Reconstruction, China-Japan Friendship Hospital, Beijing, China[5]Department of Anaesthesia and Intensive Care, Peter Hung Pain Research Institute, The Chinese University of Hong Kong, Hong Kong, China[6]State Key Laboratory of Digestive Disease, LKS Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong, China[7]Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong, China
Objectives Guillain-Barre syndrome (GBS) results from autoimmune attack on the peripheral nerves, causing sensory, motor and autonomic abnormalities. Emerging evidence suggests that there might be an association between COVID-19 and GBS. Nevertheless, the underlying pathophysiological mechanism remains unclear. Materials and Methods We performed bioinformatic analyses to delineate the potential genetic crosstalk between COVID-19 and GBS. Results COVID-19 and GBS were associated with a similar subset of immune/inflammation regulatory genes, including TNF, CSF2, IL2RA, IL1B, IL4, IL6 and IL10. Protein-protein interaction network analysis revealed that the combined gene set showed an increased connectivity as compared to COVID-19 or GBS alone, particularly the potentiated interactions with CD86, IL23A, IL27, ISG20, PTGS2, HLA-DRB1, HLA-DQB1 and ITGAM, and these genes are related to Th17 cell differentiation. Transcriptome analysis of peripheral blood mononuclear cells from patients with COVID-19 and GBS further demonstrated the activation of interleukin-17 signalling in both conditions. Conclusions Augmented Th17 cell differentiation and cytokine response was identified in both COVID-19 and GBS. PBMC transcriptome analysis also suggested the pivotal involvement of Th17 signalling pathway. In conclusion, our data suggested aberrant Th17 cell differentiation as a possible mechanism by which COVID-19 can increase the risk of GBS.
基金：
National Natural Science Foundation of China (NSFC)National Natural Science Foundation of China (NSFC) [81974354, 81772424, 81330044, 81272053]
第一作者单位：[1]Department of Orthopaedic Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China
共同第一作者：
通讯作者：
通讯机构：[1]Department of Orthopaedic Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China[2]CUHK-Shenzhen Research Institute, Shenzhen, China[5]Department of Anaesthesia and Intensive Care, Peter Hung Pain Research Institute, The Chinese University of Hong Kong, Hong Kong, China[6]State Key Laboratory of Digestive Disease, LKS Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong, China[*1]Department of Orthopaedic Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100042, China[*2]Department of Anaesthesia and Intensive Care, The Chinese University of Hong Kong, Hong Kong, China
推荐引用方式(GB/T 7714)：
Zheng Li,Ziheng Huang,Xingye Li,et al.Bioinformatic analyses hinted at augmented T helper 17 cell differentiation and cytokine response as the central mechanism of COVID-19-associated Guillain-Barre syndrome[J].CELL PROLIFERATION.2021,54(5):doi:10.1111/cpr.13024.
APA：
Zheng Li,Ziheng Huang,Xingye Li,Cheng Huang,Jianxiong Shen...&William Ka Kei Wu.(2021).Bioinformatic analyses hinted at augmented T helper 17 cell differentiation and cytokine response as the central mechanism of COVID-19-associated Guillain-Barre syndrome.CELL PROLIFERATION,54,(5)
MLA：
Zheng Li,et al."Bioinformatic analyses hinted at augmented T helper 17 cell differentiation and cytokine response as the central mechanism of COVID-19-associated Guillain-Barre syndrome".CELL PROLIFERATION 54..5(2021)
生物学