| Title | Bioinformatic analyses hinted at augmented T helper 17 cell differentiation and cytokine response as the central mechanism of COVID-19-associated Guillain-Barre syndrome |
| Authors | Li, Zheng Huang, Ziheng Li, Xingye Huang, Cheng Shen, Jianxiong Li, Shugang Zhang, Lin Wong, Sunny H. Chan, Matthew T., V Wu, William Ka Kei |
| Affiliation | Chinese Acad Med Sci & Peking Union Med Coll, Peking Union Med Coll Hosp, Dept Orthopaed Surg, Beijing 100042, Peoples R China CUHK Shenzhen Res Inst, Shenzhen, Peoples R China Peking Univ, Jishuitan Orthopaed Coll, Beijing Jishuitan Hosp, Dept Orthoped Surg,Clin Coll 4,Tsinghua Univ, Beijing, Peoples R China China Japan Friendship Hosp, Ctr Osteonecrosis & Joint Preserving & Reconstruc, Dept Orthopaed Surg, Beijing, Peoples R China Chinese Univ Hong Kong, Peter Hung Pain Res Inst, Dept Anaesthesia & Intens Care, Hong Kong, Peoples R China Chinese Univ Hong Kong, LKS Inst Hlth Sci, State Key Lab Digest Dis, Hong Kong, Peoples R China Chinese Univ Hong Kong, Dept Med & Therapeut, Hong Kong, Peoples R China |
| Issue Date | Mar-2021 |
| Publisher | CELL PROLIFERATION |
| Abstract | 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. |
| URI | http://hdl.handle.net/20.500.11897/610235 |
| ISSN | 0960-7722 |
| DOI | 10.1111/cpr.13024 |
| Indexed | SCI(E) |
| Appears in Collections: | 北京积水潭医院 |
