High expression of IL6 and decrease in immune cells in COVID-19 patients combined with myocardial injury

Area of Science:

• Cardiology
• Immunology
• Infectious Diseases

Background:

• Myocardial injury is a significant complication of coronavirus disease-2019 (COVID-19), leading to adverse outcomes.
• Identifying key regulatory molecules in COVID-19-related myocardial injury is crucial for developing effective treatments and improving patient prognosis.

Purpose of the Study:

• To identify key regulatory molecules and pathways involved in myocardial injury associated with COVID-19.
• To explore the relationship between specific molecular markers, immune cell populations, and myocardial injury in COVID-19 patients.

Main Methods:

• Utilized Gene Set Enrichment Analysis (GSEA) to identify co-regulatory pathways and screened differentially expressed genes (DEGs).
• Constructed a protein-protein interaction (PPI) network to identify key regulatory genes and validated findings across multiple datasets.
• Analyzed clinical data from 267 COVID-19 patients, including high-sensitivity troponin (hsTnI) levels, interleukin-6 (IL6) expression, and lymphocyte subsets.

Main Results:

• The interleukin signaling pathway and GPCR ligand binding were identified as co-regulatory pathways in COVID-19-associated myocardial injury.
• Seven key genes, including IL6, were identified that distinguish patients with myocardial injury from those without.
• COVID-19 patients with myocardial injury exhibited elevated IL6 levels and decreased counts of CD4+ T cells, CD8+ T cells, B cells, and NK cells.

Conclusions:

• Myocardial injury in COVID-19 is associated with increased IL6 expression and reduced lymphocyte counts.
• Interleukin-6 (IL6) likely plays a role in mediating myocardial injury through the interleukin signaling pathway.
• Findings suggest IL6 and associated pathways as potential targets for therapeutic intervention in COVID-19 patients with myocardial injury.