SynthesisCommunications biology2025
Systemic cytokines drive conserved severity-associated myeloid responses across bacterial and viral infections.
Synthesis in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Integrated Transcriptomic and Proteomic Analysis of the Pathogenic Mechanisms ofAnimals : an open access journal from MDPI · 2026Article
- Article
- Disruption of neutrophil homeostasis is associated with functional alterations in mitochondria of critically ill COVID-19 patients.Scientific reports · 2026Article
- Dynamic monitoring of a core pro-inflammatory cytokine panel improves mortality prediction in severe influenza.Frontiers in immunology · 2026Article
- Decoding immune low-response states in sepsis: single-cell and 3D spatial transcriptomic insights into immunoparalysis.Frontiers in immunology · 2025Review
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Both bacterial and viral infections can trigger an overwhelming host response, leading to immunopathology and organ dysfunction. Multiple studies have reported dysregulated myeloid cell states in patients with bacterial sepsis or severe SARS-CoV-2 infection. However, their relevance to viral infections other than COVID-19, the factors driving their induction, and their role in tissue injury remain poorly understood. Here, we performed a multi-cohort analysis of single cell and bulk transcriptomic data from 1845 patients across 25 studies. Our meta-analysis revealed a conserved severity-associated gene signature pointing to emergency myelopoiesis (EM) and increased IL1R2 expression in monocytes and neutrophils from patients with bacterial sepsis, COVID-19, and influenza. Analysis of tocilizumab-treated COVID-19 patients showed that IL-6 signaling blockade partially reduces this signature and results in a compensatory increase in G-CSF. To validate the role of these cytokines in vivo, we used a mouse model of influenza infection that recapitulates severity-associated increases in IL1R2+ monocytes and IL1R2
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