Evidence map›Paper›PMID 40980495›Full record

ArticleDiscovery immunology2025

PROS1 released by lung basal cells limits inflammation in epithelial and monocytes during SARS-CoV-2 infection.

Theodoros Simakou, Agnieszka M Szemiel, Lucy MacDonald, Karen Kerr, Domenico Somma, Katy Diallo, Jack Frew, Olympia M Hardy, Marcus Doohan, Aziza Elmesmari and 5 more

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PubMed Full text at PMC Publisher
In one paragraph

Article in Discovery immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. The genetics of protein S deficiency: unresolved questions and new leads.Research and practice in thrombosis and haemostasis · 2026
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors.

Theodoros SimakouSchool of infection and Immunity, University of Glasgow, Glasgow, UK.ORCID https://orcid.org/0000-0002-0839-6383
Agnieszka M SzemielCVR-CRUSH, Medical Research Council, University of Glasgow Centre for Virus Research, Glasgow, UK.
Lucy MacDonaldSchool of infection and Immunity, University of Glasgow, Glasgow, UK.
Karen KerrCVR-CRUSH, Medical Research Council, University of Glasgow Centre for Virus Research, Glasgow, UK.
Domenico SommaSchool of infection and Immunity, University of Glasgow, Glasgow, UK.
Katy DialloSchool of infection and Immunity, University of Glasgow, Glasgow, UK.
Jack FrewSchool of infection and Immunity, University of Glasgow, Glasgow, UK.
Olympia M HardySchool of infection and Immunity, University of Glasgow, Glasgow, UK.
Marcus DoohanSchool of infection and Immunity, University of Glasgow, Glasgow, UK.
Aziza ElmesmariSchool of infection and Immunity, University of Glasgow, Glasgow, UK.
Charles McSharrySchool of infection and Immunity, University of Glasgow, Glasgow, UK.
Stefano AliverniniImmunology Research Core Facility, Gemelx1li Science and Technology Park, Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy.
Thomas D OttoSchool of infection and Immunity, University of Glasgow, Glasgow, UK.
Arvind H PatelCVR-CRUSH, Medical Research Council, University of Glasgow Centre for Virus Research, Glasgow, UK.
Mariola Kurowska-StolarskaSchool of infection and Immunity, University of Glasgow, Glasgow, UK.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Factors regulating the severity of pneumonitis during viral infections remain unresolved. We previously found higher expression of protein S (PROS1) in lung epithelium of mild compared to severe coronavirus disease 2019 (COVID-19) patients. We hypothesized that PROS1 may protect the upper airways by regulating epithelial and myeloid cell responses during severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Methods: To test this, Results: We found that PROS1 is present in the basal cells of healthy pseudostratified epithelium and is released during SARS-CoV-2 infection through an IFN-mediated process. Transcriptome analysis revealed that PROS1 downregulated the SARS-CoV-2-induced proinflammatory phenotypes of basal cells, transforming pathogenic CXCL10/11 Conclusion: These findings highlight the crucial role of PROS1 in protecting against severe lung pathology caused by SARS-CoV-2, by reducing epithelial- and monocyte-derived inflammation, promoting pro-repair epithelial phenotypes, and enhancing antigen presentation in myeloid cells.

Indexed as

epithelial cellinflammationmacrophagePROS1viral

Identifiers

PMID40980495
PMCPMC12448451

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.