Evidence map›Paper›PMID 39487493›Full record

ArticleJournal of inflammation (London, England)2024

Influence and distinctions of particulate matter exposure across varying etiotypes in chronic obstructive pulmonary disease (COPD) mouse model.

Jung Hur, Chin Kook Rhee, Hyoung Kyu Yoon, Chan Kwon Park, Jeong Uk Lim, Tai Joon An, Joon Young Choi, Yong Suk Jo

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of inflammation (London, England), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

8 authors.

Jung HurDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, College of Medicine, Seoul St. Mary's Hospital, The Catholic University of Korea, Seoul, South Korea.
Chin Kook RheeDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, College of Medicine, Seoul St. Mary's Hospital, The Catholic University of Korea, Seoul, South Korea.
Hyoung Kyu YoonDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Yeouido St Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, South Korea.
Chan Kwon ParkDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Yeouido St Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, South Korea.
Jeong Uk LimDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Yeouido St Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, South Korea.
Tai Joon AnDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Yeouido St Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, South Korea.
Joon Young ChoiDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Incheon St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, South Korea.
Yong Suk JoDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, College of Medicine, Seoul St. Mary's Hospital, The Catholic University of Korea, Seoul, South Korea. lucidyonge@catholic.ac.kr.

Funding

National Research Foundation of Korea NRF-2022R1I1A1A01063654
6 · The paper itself

Abstract

backgroundAir pollution, notably particulate matter (PM), significantly impacts chronic respiratory disease such chronic obstructive pulmonary disease (COPD). Although asthma-COPD overlap (ACO), considered one of the COPD etiotype, is associated with greater severity in both symptoms and outcomes, effects of PM exposure remain unclear. Thus, this study aimed to evaluate impact of PM on chronic airway disease animal models.

methodsWe established two distinct COPD etiotypes, cigarette smoking-related COPD (COPD-C) and COPD with asthma (COPD-A), using porcine pancreatic elastase (PPE) for COPD-C and a combination of PPE with ovalbumin for COPD-A. To reflect smoking influence, cigarette smoking extract was administered to both disease models. To assess impact of PM exposure, bronchoalveolar lavage fluid (BALF), proinflammatory cytokines, lung histology, and cellular damage mechanisms were analyzed.

resultsIn the COPD-A model, cell counts and type 2 cytokines were elevated in BALF independent of PM exposure. All models exhibited increased lung inflammation and emphysema due to PM exposure. Expression levels of apoptosis-related protein B-cell lymphoma protein 2 (Bcl-2) associated X (Bax) showed an inclination to increase with PM exposure. In the COPD-A model, decreased expression of basal nuclear factor erythroid-derived 2-like 2 (Nrf-2) and increased production of reactive oxygen species (ROS) due to PM exposure were noted.

conclusionWe developed two distinct models for the etiotypes of COPD and found increased vulnerability to cell damage in COPD-A after PM exposure. Moreover, the control group displayed escalated airway inflammation and emphysema due to PM exposure, substantiating the risk of respiratory diseases.

Indexed as

AsthmaChronic obstructive pulmonary diseaseOxidative stressParticulate matter

Identifiers

PMID39487493
PMCPMC11529024

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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.