Baricitinib attenuates the proinflammatory phase of COVID-19 driven by lung-infiltrating monocytes
Open accessAbstract
SARS-CoV-2-infected subjects are generally asymptomatic during initial viral replication but may suffer severe immunopathology after the virus has receded and monocytes have infiltrated the airways. In bronchoalveolar lavage fluid from severe COVID-19 patients, monocytes express mRNA encoding inflammatory mediators and contain SARS-CoV-2 transcripts. We leverage a human small airway model of infection and inflammation, whereby primary blood monocytes transmigrate across SARS-CoV-2-infected lung epithelium to characterize viral burden, gene expression, and inflammatory mediator secretion by epithelial cells and monocytes. In this model, lung-infiltrating monocytes acquire SARS-CoV-2 from the epithelium and upregulate expression and secretion of inflammatory mediators, mirroring in vivo data. Combined use of baricitinib (Janus kinase inhibitor) and remdesivir (nucleoside analog) enhances antiviral signaling and viral clearance by SARS-CoV-2-positive monocytes while decreasing secretion of proneutrophilic mediators associated with acute respiratory distress syndrome. These findings highlight the role of lung-infiltrating monocytes in COVID-19 pathogenesis and their importance as a therapeutic target.
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Inhibition of pro-inflammatory JAK signalling in the same model attenuated pathogenesis by reducing monocyte infiltration to the lung.
“Similarly, the inhibition of pro-inflammatory JAK signalling in the same model was shown to attenuate pathogenesis by reducing the infiltration of monocytes to the lung130–132.”
From COVID-19 and cellular senescence (2023) · cites this paper as [132]
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References 58 · Cited by 19
- Authors
- Dobosh, B., Zandi, K., Giraldo, D. M., Goh, S. L., Musall, K., Aldeco, M., LeCher, J., Giacalone, V. D., Yang, J., Eddins, D. J., Bhasin, M., Ghosn, E., Sukhatme, V., Schinazi, R. F., & Tirouvanziam, R.
- Affiliations
- Emory University (US)
- Corresponding author
- Tirouvanziam, Rabindra
- ORCID
- Venue
- Cell Reports
- Publisher
- Elsevier BV
- Published
- 2022-06
- Volume
- 39
- Issue
- 11
- Pages
- 110945
- ISSN
- 2211-1247 (ISSN-L)
- PMC
- PMC9130711
- OpenAlex
- W4281562837
- Cited by
- 19
- References
- 58
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 6 · 2023: 3 · 2022: 5
- FWCI
- 2.20
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cell Reports (publishedVersion, cc-by)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- NIMH (R01MH116695)
- University of Maryland
- Children's Healthcare of Atlanta
- National Science Foundation (2032273)
- Winship Cancer Institute
- National Institutes of Health
- Topics
- Health Sciences › Medicine › Infectious Diseases › COVID-19 Clinical Research Studies
- Health Sciences › Medicine › Infectious Diseases › SARS-CoV-2 and COVID-19 Research
- Life Sciences › Immunology and Microbiology › Immunology › Inflammation biomarkers and pathways
- Keywords
- baricitinib, COVID-19 pandemic, SARS-CoV-2, monocyte transmigration, bronchoalveolar lavage, inflammatory mediators, acute respiratory distress syndrome, neutrophilic inflammation, remdesivir, viral clearance, Janus kinase inhibition, antiviral signaling
- MeSH terms
- SARS-CoV-2, COVID-19 Drug Treatment, Azetidines, Humans, Lung, Monocytes, Purines, Pyrazoles, Sulfonamides, Inflammation Mediators
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