Evidence map›Paper›PMID 39439801›Full record

ArticleFrontiers in immunology2024

Inflammatory profile of eosinophils in asthma-COPD overlap and eosinophilic COPD: a multi-omics study.

Keeya Sunata, Jun Miyata, Yusuke Kawashima, Ryo Konno, Masaki Ishikawa, Yoshinori Hasegawa, Ryuta Onozato, Yo Otsu, Emiko Matsuyama, Hisashi Sasaki and 7 more

Abstract read
In one paragraph

Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed.

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  9. [Pathological roles of lipid metabolism disorders in asthma and related intervention strategies].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026
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  18. Plasma Levels of CXCL9 and MCP-3 are Increased in Asthma-COPD Overlap (ACO) Patients.International journal of chronic obstructive pulmonary disease · 2025
    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

17 authors.

Keeya SunataDivision of Pulmonary Medicine, Department of Medicine, Keio University School of Medicine, Tokyo, Japan.
Jun MiyataDivision of Pulmonary Medicine, Department of Medicine, Keio University School of Medicine, Tokyo, Japan.
Yusuke KawashimaDepartment of Applied Genomics, Kazusa DNA Research Institute, Chiba, Japan.
Ryo KonnoDepartment of Applied Genomics, Kazusa DNA Research Institute, Chiba, Japan.
Masaki IshikawaDepartment of Applied Genomics, Kazusa DNA Research Institute, Chiba, Japan.
Yoshinori HasegawaDepartment of Applied Genomics, Kazusa DNA Research Institute, Chiba, Japan.
Ryuta OnozatoDivision of Pulmonary Medicine, Department of Medicine, Keio University School of Medicine, Tokyo, Japan.
Yo OtsuDivision of Pulmonary Medicine, Department of Medicine, Keio University School of Medicine, Tokyo, Japan.
Emiko MatsuyamaDivision of Pulmonary Medicine, Department of Medicine, Keio University School of Medicine, Tokyo, Japan.
Hisashi SasakiDivision of Infectious Diseases and Respiratory Medicine, Department of Internal Medicine, National Defense Medical College, Saitama, Japan.
Shinichi OkuzumiDivision of Pulmonary Medicine, Department of Medicine, Keio University School of Medicine, Tokyo, Japan.
Takao MochimaruDivision of Pulmonary Medicine, Department of Medicine, Keio University School of Medicine, Tokyo, Japan.
Katsunori MasakiDivision of Pulmonary Medicine, Department of Medicine, Keio University School of Medicine, Tokyo, Japan.
Hiroki KabataDivision of Pulmonary Medicine, Department of Medicine, Keio University School of Medicine, Tokyo, Japan.
Shotaro ChubachiDivision of Pulmonary Medicine, Department of Medicine, Keio University School of Medicine, Tokyo, Japan.
Makoto AritaLaboratory for Metabolomics, RIKEN Center for Integrative Medical Sciences, Kanagawa, Japan.
Koichi FukunagaDivision of Pulmonary Medicine, Department of Medicine, Keio University School of Medicine, Tokyo, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Elevated blood eosinophil levels in patients with chronic obstructive pulmonary disease (COPD) with or without asthma are linked to increased exacerbations and the effectiveness of inhaled corticosteroid treatment. This study aimed to delineate the inflammatory cellular properties of eosinophils in patients with asthma-COPD overlap (ACO) and eosinophilic COPD (eCOPD). Methods: Eosinophils were isolated from the peripheral blood of healthy volunteers, patients with non-eCOPD, and those with ACO/eCOPD. Multi-omics analysis involving transcriptomics, proteomics, and lipidomics was performed, followed by bioinformatic data analyses. In vitro experiments using eosinophils from healthy volunteers were conducted to investigate the molecular mechanisms underlying cellular alterations in eosinophils. Results: Proteomics and transcriptomics analyses revealed cellular characteristics in overall COPD patients represented by viral infection (elevated expression of sterol regulatory element-binding protein-1) and inflammatory responses (elevated levels of IL1 receptor-like 1, Fc epsilon receptor Ig, and transmembrane protein 176B). Cholesterol metabolism enzymes were identified as ACO/eCOPD-related factors. Gene Ontology and pathway enrichment analyses demonstrated the key roles of antiviral responses, cholesterol metabolism, and inflammatory molecules-related signaling pathways in ACO/eCOPD. Lipidomics showed the impaired synthesis of cyclooxygenase-derived mediators including prostaglandin E2 (PGE2) in ACO/eCOPD. In vitro assessment confirmed that IL-33 or TNF-α stimulation combined with IL-5 and IFN-γ stimulation induced cellular signatures in eosinophils in ACO/eCOPD. Atorvastatin, dexamethasone, and PGE2 differentially modulated these inflammatory changes. Discussion: ACO/eCOPD is associated with viral infection and an inflammatory milieu. Therapeutic strategies using statins and inhaled corticosteroids are recommended to control these pathogenic changes.

Indexed as

EosinophilsPulmonary Disease, Chronic ObstructiveAgedAsthmaAsthma-Chronic Obstructive Pulmonary Disease Overlap SyndromeFemaleGene Expression ProfilingHumansInflammationLipidomicsMaleMiddle AgedMultiomicsProteomicsPulmonary EosinophiliaTranscriptomeasthma-COPD overlapchronic obstructive pulmonary diseaseeosinophilIL-33interferon-γmulti-omicsstatintumor necrosis factor-α

Identifiers

PMID39439801
PMCPMC11493663

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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.