Journal
FRONTIERS IN IMMUNOLOGY
Volume 14, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2023.1157179
Keywords
COVID-19; lung-brain axis; long COVID; brain damage; sequelae; TIMP 1; RPS 29
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This study aimed to explore the critical molecular and immune infiltration situations in the brain of elderly COVID-19 patients. The results revealed the enrichment in synapse and neuroactive ligand-receptor interaction in COVID-19 patients, as well as the imbalance of immune infiltration, including CD8+ T cells, neutrophils, and HLA. RPS29, S100A10, and TIMP1 were identified as critical genes contributing to the progress of brain damage.
IntroductionAlthough many studies have demonstrated the existing neurological symptoms in COVID-19 patients, the mechanisms are not clear until now. This study aimed to figure out the critical molecular and immune infiltration situations in the brain of elderly COVID-19 patients. MethodsGSE188847 was used for the differential analysis, WGCNA, and immune infiltration analysis. We also performed GO, KEGG, GSEA, and GSVA for the enrich analysis. Results266 DEGs, obtained from the brain samples of COVID-19 and non-COVID-19 patients whose ages were over 70 years old, were identified. GO and KEGG analysis revealed the enrichment in synapse and neuroactive ligand-receptor interaction in COVID-19 patients. Further analysis found that asthma and immune system signal pathways were significant changes based on GSEA and GSVA. Immune infiltration analysis demonstrated the imbalance of CD8+ T cells, neutrophils, and HLA. The MEpurple module genes were the most significantly different relative to COVID-19. Finally, RPS29, S100A10, and TIMP1 were the critical genes attributed to the progress of brain damage. ConclusionRPS29, S100A10, and TIMP1 were the critical genes in the brain pathology of COVID-19 in elderly patients. Our research has revealed a new mechanism and a potential therapeutic target.
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