What question did this study set out to answer?

This research aims to identify transcriptomic and immune signatures that differentiate the need for invasive mechanical ventilation in COVID-19 related ARDS patients.

May 20, 2026

A108-03 Integrated Transcriptomic and Immune Profiling to Predict Respiratory Failure in COVID-19 ARDS

Key Points

This research aims to identify transcriptomic and immune signatures that differentiate the need for invasive mechanical ventilation in COVID-19 related ARDS patients.
Enrolled 36 patients with SARS-CoV-2 infection requiring oxygen support.
Collected blood samples at baseline, day 4, and day 8 from IMV (n=14) and non-IMV (n=22) groups.
Assessed transcriptomic profiles using RNA-sequencing and measured plasma cytokines with multiplex immunoassays.
Patients on IMV had longer hospital stays (43 vs 19 days, p=0.01) and higher 28-day mortality (45% vs 12%; aOR=8.78, p=0.04).
Identified 36 differentially expressed genes at day 4 and 21 genes at day 8 in IMV patients, including significant upregulation of stress-response genes and downregulation of mitochondrial genes (p<0.05).
Plasma IL-10 showed strong predictive value for IMV need (AUC 0.74, p=0.0002).

Abstract

Abstract Rationale Severe COVID-19-related acute respiratory distress syndrome (ARDS) often progresses to respiratory failure requiring invasive mechanical ventilation (IMV). Although several biomarkers (e.g., CRP, suPAR, Ang-2) have been explored to predict COVID-19 disease severity, validated early-presentation biomarkers that specifically prognosticate the need for IMV in ARDS remain limited. Reliable prognostic tools would help clinicians identify high-risk patients for closer monitoring and inform resource allocation. Research Question What transcriptomic and immune signatures distinguish IMV from non-IMV in patients with COVID-19 ARDS, and how do these molecular changes contribute to disease severity? Methods Patients (n = 36) with SARS-CoV-2 infection requiring oxygen support were enrolled in this prospective study. Blood samples were collected at baseline, day 4, and day 8 from patients on IMV (n = 14) and non-IMV (n = 22). Transcriptomic profiles of peripheral blood mononuclear cells were assessed using RNA-sequencing, followed by gene ontology and KEGG pathway enrichment. Plasma cytokines and chemokines were measured using multiplex immunoassays, peripheral immune cell endotypes were characterized by mass cytometry, and neutrophil extracellular trap (NET) formation was evaluated by kinetic live-cell imaging. Results Clinically, IMV patients had significantly longer hospital (43 vs 19 days, p = 0.01) and ICU stays (39.6 vs 9.1 days, p 0.001) and higher 28-day mortality (45% vs 12%; aOR = 8.78, p = 0.04). Transcriptomic profiling identified 36 differentially expressed genes (DEGs) at day 4 and 21 DEGs at day 8 in patients on IMV, characterized by downregulation of mitochondrial gene MTARC2 and anticoagulant regulator TFPI, and upregulation of stress-response genes (RNF165, KCNMA1, and AC245014.3) (p 0.05). Plasma IL-6, IL-8, and IL-10 were elevated in IMV group, with IL-10 showing the strongest predictive value (AUC 0.74, p = 0.0002). Immune profiling revealed higher precent of CD57− NK cells at baseline in non-IMV group. NET formation did not differ between groups. Conclusion These findings suggest that mitochondrial gene expression patterns, plasma IL-10 levels, and NK cell phenotypes may serve as candidate biomarkers for early risk stratification and offer mechanistic insights into pathways driving respiratory failure in COVID-19 ARDS. This abstract is funded by: 2020 Chest Foundation GlaxoSmithKline Distinguished Scholar in Respiratory Health Grant

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