Evidence map›Paper›PMID 40234868›Full record

ArticleBiomedical engineering online2025

Transcriptomic and metabolomic insights into neutrophil activity in COPD complicated by metabolic syndrome.

Juan Li, Xue Wu, Yufen Fu, Jiliu Liu, Yao Liu, Jiahuan Li, Bomiao Qing, Yi Zhang, Jie Gao, Xiang He and 2 more

Abstract read
In one paragraph

Article in Biomedical engineering online, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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

12 authors.

Juan LiLaboratory of Allergy and Precision Medicine, Chengdu Institute of Respiratory Health, The Third People's Hospital of Chengdu, Affiliated Hospital of Southwest Jiaotong University, College of Medicine, Southwest Jiaotong University, Chengdu, China.
Xue WuClinical Medicine Department, North Sichuan Medical College, Nanchong, China.
Yufen FuDepartment of Respiratory and Critical Care Medicine, Affiliated Hospital of Southwest Medical University, Luzhou, China.
Jiliu LiuLaboratory of Allergy and Precision Medicine, Chengdu Institute of Respiratory Health, The Third People's Hospital of Chengdu, Affiliated Hospital of Southwest Jiaotong University, College of Medicine, Southwest Jiaotong University, Chengdu, China.
Yao LiuState Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Macau SAR, China.
Jiahuan LiClinical Medicine Department, North Sichuan Medical College, Nanchong, China.
Bomiao QingLaboratory of Allergy and Precision Medicine, Chengdu Institute of Respiratory Health, The Third People's Hospital of Chengdu, Affiliated Hospital of Southwest Jiaotong University, College of Medicine, Southwest Jiaotong University, Chengdu, China.
Yi ZhangLaboratory of Allergy and Precision Medicine, Chengdu Institute of Respiratory Health, The Third People's Hospital of Chengdu, Affiliated Hospital of Southwest Jiaotong University, College of Medicine, Southwest Jiaotong University, Chengdu, China.
Jie GaoLaboratory of Allergy and Precision Medicine, Chengdu Institute of Respiratory Health, The Third People's Hospital of Chengdu, Affiliated Hospital of Southwest Jiaotong University, College of Medicine, Southwest Jiaotong University, Chengdu, China.
Xiang HeLaboratory of Allergy and Precision Medicine, Chengdu Institute of Respiratory Health, The Third People's Hospital of Chengdu, Affiliated Hospital of Southwest Jiaotong University, College of Medicine, Southwest Jiaotong University, Chengdu, China. xiangge530@hotmail.com.
Junyi WangLaboratory of Allergy and Precision Medicine, Chengdu Institute of Respiratory Health, The Third People's Hospital of Chengdu, Affiliated Hospital of Southwest Jiaotong University, College of Medicine, Southwest Jiaotong University, Chengdu, China. wjy520wjy@163.com.
Guoping LiLaboratory of Allergy and Precision Medicine, Chengdu Institute of Respiratory Health, The Third People's Hospital of Chengdu, Affiliated Hospital of Southwest Jiaotong University, College of Medicine, Southwest Jiaotong University, Chengdu, China. lzlgp@163.com.

Funding

National Natural Science Foundation of China 82200079National Natural Science Foundation of China 82370022National Natural Science Foundation of China 82370023
6 · The paper itself

Abstract

objectivesChronic obstructive pulmonary disease (COPD) frequently coexists with metabolic syndrome (MS), compounding its impact on patients' health and quality of life. This study aimed to elucidate the immune and metabolic response characteristics in COPD patients with and without MS.

methodsA total of 11,315 COPD patients admitted to the Department of Respiratory and Critical Care Medicine at the Third People's Hospital of Chengdu between January 1, 2013, and May 1, 2023, were selected. Multivariate logistic regression was conducted to identify the risk factors for acute exacerbation of chronic obstructive pulmonary disease. Moreover, from this cohort, 30 patients (18 with COPD and 12 with COPD-MS) were recruited for a further study to investigate the underlying mechanisms of COPD and COPD-MS. Blood samples were collected from these participants to perform transcriptomic and metabolomic analyses, aiming to explore the differences in immune responses and metabolic alterations between the two groups.

resultsOur findings indicate a significant enhancement of neutrophil-mediated immune responses in COPD-MS patients. Transcriptomic analysis revealed 327 differentially expressed genes (DEGs) significantly involved in neutrophil-mediated immunity. Key metabolic pathways were disrupted, with 39 differential metabolites identified. Notably, metabolites, such as L-homoarginine and diethanolamine, which were elevated in COPD-MS patients, showed strong correlations with DEGs involved in neutrophil pathways and immune checkpoint regulation. The study also found decreased levels of IL4 and IL5RA in COPD-MS patients, suggesting a shift from Th2 to Th1 inflammatory responses, potentially contributing to glucocorticoid resistance.

conclusionsCOPD patients with metabolic syndrome exhibit a heightened neutrophil-mediated inflammatory response and significant metabolic disturbances, which underscores the need for precise therapeutic strategies targeting both metabolic and inflammatory pathways to improve patient outcomes and manage COPD-MS complexities effectively.

Indexed as

Gene Expression ProfilingMetabolic SyndromeMetabolomeMetabolomicsNeutrophilsPulmonary Disease, Chronic ObstructiveTranscriptomeAgedFemaleHumansMaleMiddle AgedCOPDMetabolic syndromeMetabolomicsNeutrophilsTranscriptomics

Identifiers

PMID40234868
PMCPMC11998468

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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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 Socratic graph.