Bioinformatic analyses hinted at augmented T helper 17 cell differentiation and cytokine response as the central mechanism of COVID‐19–associated Guillain‐Barré syndrome
Autor: | Zheng Li, Matthew T. V. Chan, Xingye Li, Shugang Li, Sunny H. Wong, Ziheng Huang, Cheng Huang, Lin Zhang, Jianxiong Shen, William K.K. Wu |
---|---|
Rok vydání: | 2021 |
Předmět: |
0301 basic medicine
Cellular differentiation macrophage Biology Guillain-Barre Syndrome Peripheral blood mononuclear cell SARS‐CoV‐2 Transcriptome 03 medical and health sciences 0302 clinical medicine Immune system COVID‐19 Humans T helper 17 cell Gene Regulatory Networks Protein Interaction Maps Interleukin 4 CD86 SARS-CoV-2 COVID-19 Computational Biology Cell Differentiation Original Articles Cell Biology General Medicine Interleukin 10 030104 developmental biology 030220 oncology & carcinogenesis Immunology Interleukin-23 Subunit p19 Leukocytes Mononuclear Cytokines Th17 Cells Original Article Guillain‐Barré syndrome B7-2 Antigen Signal Transduction |
Zdroj: | Cell Proliferation |
ISSN: | 1365-2184 0960-7722 |
Popis: | 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. Functional protein‐protein association networks of (A) COVID‐19– and (B) GBS‐related genes were analyzed by STRING. Genes associated with the two disease entities (COVID‐19, disease id: C000657245, version 4, N.PMIDs ≥ 4; GBS, disease id: C0018378, Gene‐Disease Association Score ≥ 0.02) were retrieved from DisGeNET, a knowledge platform for disease genomics. Only highly confident interactions derived from ‘Experiments’, ‘Databases’, ‘Co‐expression’ and ‘Co‐occurrence’ with the minimum required interaction score of 0.900 were shown. The Markov cluster (MLC) algorithm with an inflation parameter of 3 was used for network clustering. |
Databáze: | OpenAIRE |
Externí odkaz: |