Bioinformatic analyses hinted at augmented T helper 17 cell differentiation and cytokine response as the central mechanism of COVID-19-associated Guillain-Barré syndrome.

Abstract

OBJECTIVES:

Guillain-Barré 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.

• Authors: Zheng Li, Ziheng Huang, Xingye Li, Cheng Huang, Jianxiong Shen, Shugang Li, Lin Zhang, Sunny H Wong, Matthew T V Chan, William Ka Kei Wu
• Journal: Cell proliferation (Cell Prolif) Vol. 54 Issue 5 Pg. e13024 (May 2021) ISSN: 1365-2184 [Electronic] England
• PMID: 33751722 (Publication Type: Journal Article)
• Copyright: © 2021 The Authors. Cell Proliferation Published by John Wiley & Sons Ltd.

Chemical References

• B7-2 Antigen
• Cytokines
• IL23A protein, human
• Interleukin-23 Subunit p19

Topics

• B7-2 Antigen (metabolism)
• COVID-19 (complications, pathology, virology)
• Cell Differentiation
• Computational Biology (methods)
• Cytokines (metabolism)
• Gene Regulatory Networks
• Guillain-Barre Syndrome (etiology, metabolism, pathology)
• Humans
• Interleukin-23 Subunit p19 (metabolism)
• Leukocytes, Mononuclear (cytology, metabolism)
• Protein Interaction Maps
• SARS-CoV-2 (isolation & purification)
• Signal Transduction
• Th17 Cells (cytology, immunology, metabolism)