Evidence map›Paper›PMID 36848564›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2023

Innate immune cell activation causes lung fibrosis in a humanized model of long COVID.

Lu Cui, Zhuoqing Fang, Cristabelle Madona De Souza, Tristan Lerbs, Yuan Guan, Irene Li, Vivek Charu, Shih-Yu Chen, Irving Weissman, Gerlinde Wernig

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
9.3field-weighted citation impact, top 1% of its field
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

30 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
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  11. Animal models of Long Covid: A hit-and-run disease.Science translational medicine · 2024
    Review
  12. Translating insights into therapies for Long Covid.Science translational medicine · 2024
    Review
  13. Review
  14. Article
  15. Article
  16. The role of the cytoskeleton in fibrotic diseases.Frontiers in cell and developmental biology · 2024
    Review
  17. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 2 countries.

Lu CuiDepartment of Pathology, Institute of Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305.ORCID 0000-0002-3531-8102
Zhuoqing FangDepartment of Anesthesiology, Pain and Perioperative Medicine, Stanford University School of Medicine, Stanford, CA 94305.ORCID 0000-0002-7418-1313
Cristabelle Madona De SouzaDepartment of Pathology, Institute of Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305.
Tristan LerbsDepartment of Pathology, Institute of Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305.
Yuan GuanDepartment of Anesthesiology, Pain and Perioperative Medicine, Stanford University School of Medicine, Stanford, CA 94305.
Irene LiDepartment of Biomedical Data Science, Stanford University School of Medicine, Stanford, CA 94305.
Vivek CharuDepartment of Pathology, Institute of Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305.
Shih-Yu ChenInstitute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan.ORCID 0000-0002-7955-481X
Irving WeissmanDepartment of Pathology, Institute of Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305.ORCID 0000-0002-9077-7467
Gerlinde WernigDepartment of Pathology, Institute of Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305.ORCID 0000-0002-5169-8731
Stanford University · USInstitute of Biomedical Sciences, Academia Sinica · TW

Funding

Boehringer Ingelheim (BI) SPO182437National Scleroderma Foundation (SF) SPO134886
6 · The paper itself

Abstract

COVID-19 remains a global pandemic of an unprecedented magnitude with millions of people now developing "COVID lung fibrosis." Single-cell transcriptomics of lungs of patients with long COVID revealed a unique immune signature demonstrating the upregulation of key proinflammatory and innate immune effector genes CD47, IL-6, and JUN. We modeled the transition to lung fibrosis after COVID and profiled the immune response with single-cell mass cytometry in JUN mice. These studies revealed that COVID mediated chronic immune activation reminiscent to long COVID in humans. It was characterized by increased CD47, IL-6, and phospho-JUN (pJUN) expression which correlated with disease severity and pathogenic fibroblast populations. When we subsequently treated a humanized COVID lung fibrosis model by combined blockade of inflammation and fibrosis, we not only ameliorated fibrosis but also restored innate immune equilibrium indicating possible implications for clinical management of COVID lung fibrosis in patients.

Indexed as

COVID-19Pulmonary FibrosisAnimalsCD47 AntigenHumansImmunity, InnateInterleukin-6MicePost-Acute COVID-19 SyndromeCD47 AntigenInterleukin-6humanized mouse modelimmune checkpoint therapyinnate immunitylong COVID pulmonary fibrosis

Identifiers

PMID36848564
PMCPMC10013740
OpenAlexW4322490010

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.