Evidence map›Paper›PMID 40189583›Full record

ArticleInflammation and regeneration2025

CD147-high classical monocytes: a cellular biomarker for COVID-19 disease severity and treatment response.

Teruaki Murakami, Yuta Yamaguchi, Saori Amiya, Yuko Yoshimine, Shinichiro Nameki, Yasutaka Okita, Yasuhiro Kato, Haruhiko Hirata, Yoshito Takeda, Atsushi Kumanogoh and 1 more

Abstract read
In one paragraph

Article in Inflammation and regeneration, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

11 authors.

Teruaki MurakamiDepartment of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, 2-2, Yamadaoka, Suita, Osaka, 565-0871, Japan.
Yuta YamaguchiDepartment of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, 2-2, Yamadaoka, Suita, Osaka, 565-0871, Japan.
Saori AmiyaDepartment of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, 2-2, Yamadaoka, Suita, Osaka, 565-0871, Japan.
Yuko YoshimineDepartment of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, 2-2, Yamadaoka, Suita, Osaka, 565-0871, Japan.
Shinichiro NamekiDepartment of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, 2-2, Yamadaoka, Suita, Osaka, 565-0871, Japan.
Yasutaka OkitaDepartment of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, 2-2, Yamadaoka, Suita, Osaka, 565-0871, Japan.
Yasuhiro KatoDepartment of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, 2-2, Yamadaoka, Suita, Osaka, 565-0871, Japan.
Haruhiko HirataDepartment of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, 2-2, Yamadaoka, Suita, Osaka, 565-0871, Japan.
Yoshito TakedaDepartment of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, 2-2, Yamadaoka, Suita, Osaka, 565-0871, Japan.
Atsushi KumanogohDepartment of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, 2-2, Yamadaoka, Suita, Osaka, 565-0871, Japan.
Takayoshi MoritaDepartment of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, 2-2, Yamadaoka, Suita, Osaka, 565-0871, Japan. t-morita@imed3.med.osaka-u.ac.jp.ORCID http://orcid.org/0000-0002-7111-9506

Funding

Japan Agency for Medical Research and Development J200705023Japan Agency for Medical Research and Development J200705049Japan Agency for Medical Research and Development J200705710Japan Agency for Medical Research and Development JP18 cm016335Japan Agency for Medical Research and Development JP18 cm059042Japan Society for the Promotion of Science JP18H05282Japan Society for the Promotion of Science JP21K16287
6 · The paper itself

Abstract

backgroundSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection can lead to severe coronavirus disease 2019 (COVID-19), which is characterized by cytokine storm and organ dysfunction. The spike S1 subunit induces inflammatory cytokine production, but the immune cell subsets that respond to S1 stimulation and contribute to disease severity remain unclear.

methodsWe analyzed serum samples and peripheral blood mononuclear cells (PBMCs) from patients with COVID-19 (moderate: n = 7; severe: n = 25) and healthy controls (n = 38). Using mass cytometry (cytometry by time-of-flight; CyTOF), we analyzed immune cell responses to S1 subunit stimulation in PBMCs from healthy donors and patients with COVID-19. We examined correlations among identified cell populations, serum cytokine levels, and clinical parameters.

resultsSerum S1 subunit levels correlated with disease severity and inflammatory cytokine concentrations. S1 subunit stimulation induced dose-dependent cytokine production from PBMCs, predominantly from myeloid cells. CyTOF analysis identified classical monocytes with high CD147 expression (CD147hi cMono) as the primary source of S1-induced cytokines. The proportion of CD147hi cMono increased significantly in severe COVID-19 and decreased with clinical improvement. The frequency of CD147hi cMono showed a stronger positive correlation with clinical severity markers in younger patients compared to older patients.

conclusionsCD147hi cMono are the primary cellular source of S1-induced inflammatory cytokines and may serve as potential biomarkers for monitoring COVID-19 severity and treatment response.

Indexed as

CD147Classical monocyteCOVID-19Cytokine stormInflammationMass cytometrySARS-CoV-2Spike S1 subunit

Identifiers

PMID40189583
PMCPMC11974131

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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.