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Global Transcriptomic analysis of PBMC derived from COVID-19 acute-severe patients and convalescents

ABSTRACT: The majority of patients with COVID-19 have a self-limiting upper respiratory tract infection mostly represented by asymptomatic or mild, however a small but relevant proportion of patients develops acute respiratory distress syndrome (ARDS), characterised by an excessive, host immune response with overproduction of proinflammatory cytokines can rapidly lead to multi-organ failure and death. Indeed, immune pathologies are well characterised through deep immune phenotyping, plasma analysis, sc-RNA and chip based methylation analysis, still we lack a molecular understanding of immune pathologies associated with COVID-19 which is urgently needed for new prognostic and therapeutic interventions. In this study, we first time showed a SARS-Cov2 induced severity associated deregulation of immune functions driven through a global reprogramming of immune functions through a epigenetically driven gene regulatory network

ORGANISM(S): Homo sapiens

PROVIDER: GSE202805 | GEO | 2025/04/10

REPOSITORIES: GEO

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Project description:Background: COVID-19 and sepsis represent formidable public health challenges, characterized by incompletely elucidated molecular mechanisms. Elucidating the interplay between COVID-19 and sepsis, particularly in geriatric patients suffering from sepsis-induced acute respiratory distress syndrome (ARDS), is of paramount importance for identifying potential therapeutic interventions to mitigate hospitalization and mortality risks.We employed bioinformatics and systems biology approaches to identify hub genes, shared pathways, molecular biomarkers, and candidate therapeutics for managing COVID-19, sepsis, and sepsis-induced ARDS. We corroborated these hub genes utilizing murine sepsis-ARDS models and blood samples derived from geriatric patients afflicted by sepsis-induced ARDS.Results: Our investigation revealed 189 differentially expressed genes (DEGs) shared among COVID-19 and sepsis datasets. We constructed a protein-protein interaction network, unearthing pivotal hub genes and modules. Notably, nine hub genes displayed significant alterations and correlations with critical inflammatory mediators of pulmonary injury in murine septic lungs. Simultaneously, 12 displayed significant changes and correlations with a neutrophil-recruiting chemokine in geriatric patients with sepsis-induced ARDS. Of these, six hub genes (CD247, CD2, CD40LG, KLRB1, LCN2, RETN) showed significant alterations across COVID-19, sepsis, and geriatric sepsis-induced ARDS. Our single-cell RNA sequencing analysis of hub genes across 3 diverse immune cell types furnished insights into disease pathogenesis. Functional analysis underscored the interconnection between sepsis/sepsis-ARDS and COVID-19, enabling us to pinpoint potential therapeutic targets, transcription factor-gene interactions, DEG-microRNA co-regulatory networks, and prospective drug and chemical compound interactions involving hub genes.Our investigation offers potential therapeutic targets/biomarkers, sheds light on the immune response in geriatric patients with sepsis-induced ARDS, emphasizes the association between sepsis/sepsis-ARDS and COVID-19, and proposes novel avenues for targeted therapies.

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Global Transcriptomic analysis of PBMC derived from COVID-19 acute-severe patients and convalescents

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