Evidence map›Paper›PMID 39805823›Full record

ArticleNature communications2025

Neutrophil adhesion to vessel walls impairs pulmonary circulation in COVID-19 pathology.

Hiroshi Ueki, I-Hsuan Wang, Maki Kiso, Kenta Horie, Shun Iida, Sohtaro Mine, Michiko Ujie, Hung-Wei Hsu, Chen-Hui Henry Wu, Masaki Imai and 4 more

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Article
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  4. Review
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  8. Review
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

14 authors.

Hiroshi Ueki *Division of Virology, Institute of Medical Science, University of Tokyo, Tokyo, Japan. h-ueki@ims.u-tokyo.ac.jp.ORCID http://orcid.org/0000-0002-6557-0771
I-Hsuan Wang *Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.ORCID http://orcid.org/0000-0003-2159-7347
Maki KisoDivision of Virology, Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Kenta HorieDepartment of Artificial Intelligence Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.ORCID http://orcid.org/0000-0003-4175-1014
Shun IidaDepartment of Pathology, National Institute of Infectious Diseases, Tokyo, Japan.ORCID http://orcid.org/0000-0003-2258-9031
Sohtaro MineDepartment of Pathology, National Institute of Infectious Diseases, Tokyo, Japan.
Michiko UjieDivision of Virology, Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Hung-Wei HsuInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
Chen-Hui Henry WuInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.ORCID http://orcid.org/0009-0000-6303-920X
Masaki ImaiDivision of Virology, Institute of Medical Science, University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0001-6988-1975
Tadaki SuzukiDepartment of Pathology, National Institute of Infectious Diseases, Tokyo, Japan.ORCID http://orcid.org/0000-0002-3820-9542
Wataru KamitaniDepartment of Infectious Diseases and Host Defense, Gunma University Graduate School of Medicine, Gunma, Japan.
Eiryo KawakamiDepartment of Artificial Intelligence Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.ORCID http://orcid.org/0000-0001-9955-4342
Yoshihiro KawaokaDivision of Virology, Institute of Medical Science, University of Tokyo, Tokyo, Japan. yoshihiro.kawaoka@wisc.edu.ORCID http://orcid.org/0000-0001-5061-8296

Funding

Division of Intramural Research, National Institute of Allergy and Infectious Diseases (Division of Intramural Research of the NIAID) CRIP; HHSN272201400008CJapan Agency for Medical Research and Development (AMED) JP19fk0108113Japan Agency for Medical Research and Development (AMED) JP20fk0108412Japan Agency for Medical Research and Development (AMED) JP21fk0108552Japan Agency for Medical Research and Development (AMED) JP243fa627001Japan Agency for Medical Research and Development (AMED) JP24wm0125002MEXT | Japan Science and Technology Agency (JST) JPMJMS2025MEXT | Japan Society for the Promotion of Science (JSPS) 21K14984NIAID NIH HHS HHSN272201400008C
6 · The paper itself

Abstract

Microthrombus formation is associated with COVID-19 severity; however, the detailed mechanism remains unclear. In this study, we investigated mouse models with severe pneumonia caused by SARS-CoV-2 infection by using our in vivo two-photon imaging system. In the lungs of SARS-CoV-2-infected mice, increased expression of adhesion molecules in intravascular neutrophils prolonged adhesion time to the vessel wall, resulting in platelet aggregation and impaired lung perfusion. Re-analysis of scRNA-seq data from peripheral blood mononuclear cells from COVID-19 cases revealed increased expression levels of CD44 and SELL in neutrophils in severe COVID-19 cases compared to a healthy group, consistent with our observations in the mouse model. These findings suggest that pulmonary perfusion defects caused by neutrophil adhesion to pulmonary vessels contribute to COVID-19 severity.

Indexed as

COVID-19LungNeutrophilsPulmonary CirculationAnimalsCell AdhesionDisease Models, AnimalFemaleHumansHyaluronan ReceptorsMaleMiceMice, Inbred C57BLPlatelet AggregationSARS-CoV-2Hyaluronan Receptors

Identifiers

PMID39805823
PMCPMC11730596

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.