ArticleExperimental & molecular medicine2023
Corticosteroids reduce pathologic interferon responses by downregulating STAT1 in patients with high-risk COVID-19.
Article in Experimental & molecular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 13 citations in OpenAlex.
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- Development of an Integrated CE-Cell-SELEX Strategy for Rational Selection of Human Bone Microvascular Endothelial Cell Aptamers.Molecules (Basel, Switzerland) · 2026Article
- Benign Adrenal Adenomas Are Associated With Reduced Prevalence of Hospitalised Patients With COVID-19.Clinical endocrinology · 2026Article
- The Role of Type I Interferons in Tuberculosis and in Tuberculosis-Risk-Associated Comorbidities.Infectious disease reports · 2025Review
- Role of Ferroptosis in the Progression of COVID-19 and the Development of Long COVID.Current medicinal chemistry · 2025Article
- Proposed observational study protocol for early differentiation of cytokine release syndrome and sepsis in CAR-T recipients with haematological malignancies using the IL-6/PCT ratio: the DRACARYS study.Frontiers in oncology · 2025Article
- Integrative Genomic and Transcriptomic Analysis in Acute Interstitial Pneumonia.Journal of cellular and molecular medicine · 2024Article
- Article
- Global analysis of the abundance of AU-rich mRNAs in response to glucocorticoid treatment.Scientific reports · 2024Article
- Shared Immune Associations Between COVID-19 and Inflammatory Bowel Disease: A Cross-Sectional Observational Study in Shanghai, China.Journal of inflammation research · 2024Article
- Can interferon-inducible gene expression guide treatment? A prospective study in QuantiFERON-positive uveitis with undetermined cause.Taiwan journal of ophthalmologyArticle
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Authors and funding
12 authors at 7 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We do not yet understand exactly how corticosteroids attenuate hyperinflammatory responses and alleviate high-risk coronavirus disease 2019 (COVID-19). We aimed to reveal the molecular mechanisms of hyperinflammation in COVID-19 and the anti-inflammatory effects of corticosteroids in patients with high-risk COVID-19. We performed single-cell RNA sequencing of peripheral blood mononuclear cells (PBMCs) from three independent COVID-19 cohorts: cohort 1 was used for comparative analysis of high-risk and low-risk COVID-19 (47 PBMC samples from 28 patients), cohort 2 for longitudinal analysis during COVID-19 (57 PBMC samples from 15 patients), and cohort 3 for investigating the effects of corticosteroid treatment in patients with high-risk COVID-19 (55 PBMC samples from 13 patients). PBMC samples from healthy donors (12 PBMC samples from 12 donors) were also included. Cohort 1 revealed a significant increase in the proportion of monocytes expressing the long noncoding RNAs NEAT1 and MALAT1 in high-risk patients. Cohort 2 showed that genes encoding inflammatory chemokines and their receptors were upregulated during aggravation, whereas genes related to angiogenesis were upregulated during improvement. Cohort 3 demonstrated downregulation of interferon-stimulated genes (ISGs), including STAT1, in monocytes after corticosteroid treatment. In particular, unphosphorylated STAT-dependent ISGs enriched in monocytes from lupus patients were selectively downregulated by corticosteroid treatment in patients with high-risk COVID-19. Corticosteroid treatment suppresses pathologic interferon responses in monocytes by downregulating STAT1 in patients with high-risk COVID-19. Our study provides insights into the mechanisms underlying COVID-19 aggravation and improvement and the effects of corticosteroid treatment.
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