Evidence map›Paper›PMID 39160551›Full record

ArticleRespiratory research2024

Expression of human Interferon Regulatory Factor 3 (IRF-3) in alveolar macrophages relates to clinical and functional traits in COPD.

Simonetta Baraldo, Matteo Bonato, Sebastiano Cassia, Paolo Casolari, Laura De Ferrari, Mariaenrica Tiné, Federico Baraldi, Tommaso Bigoni, Anna Maria Riccio, Fulvio Braido and 3 more

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Article in Respiratory research, 2024. 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
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2citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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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.

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4 · The record

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5 · Who and what money

Authors and funding

13 authors.

Simonetta Baraldo *Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padova, Padova, Italy.
Matteo Bonato *Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padova, Padova, Italy.
Sebastiano CassiaRespiratory Clinic, Department of Internal Medicine, University of Genoa, Genoa, Italy.
Paolo CasolariSection of Respiratory Diseases, Department of Translational Medicine, University of Ferrara, Ferrara, Italy.
Laura De FerrariRespiratory Clinic, Department of Internal Medicine, University of Genoa, Genoa, Italy.
Mariaenrica TinéDepartment of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padova, Padova, Italy.
Federico BaraldiSection of Respiratory Diseases, Department of Translational Medicine, University of Ferrara, Ferrara, Italy.
Tommaso BigoniSection of Respiratory Diseases, Department of Translational Medicine, University of Ferrara, Ferrara, Italy.
Anna Maria RiccioRespiratory Clinic, Department of Internal Medicine, University of Genoa, Genoa, Italy.
Fulvio BraidoRespiratory Clinic, Department of Internal Medicine, University of Genoa, Genoa, Italy.
Marina SaettaDepartment of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padova, Padova, Italy.
Alberto PapiSection of Respiratory Diseases, Department of Translational Medicine, University of Ferrara, Ferrara, Italy.
Marco ContoliSection of Respiratory Diseases, Department of Translational Medicine, University of Ferrara, Ferrara, Italy. ctm@unife.it.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionChronic obstructive pulmonary disease (COPD) is a frequent cause of morbidity and mortality. Dysregulated and enhanced immune-inflammatory responses have been described in COPD. Recent data showed impaired immune responses and, in particular, of interferon (IFNs) signaling pathway in these patients.

aimTo evaluate in peripheral lung of COPD patients, the expression of some of the less investigated key components of the innate immune responses leading to IFN productions including: IFN-receptors (IFNAR1/IFNAR2), IRF-3 and MDA-5. Correlations with clinical traits and with the inflammatory cell profile have been assessed.

methodsLung specimens were collected from 58 subjects undergoing thoracic surgery: 22 COPD patients, 21 smokers with normal lung function (SC) and 15 non-smoker controls (nSC). The expression of IFNAR1, IFNAR2, IRF-3 and MDA-5, of eosinophils and activated NK cells (NKp46+) were quantified in the peripheral lung by immunohistochemistry.

resultsA significant increase of IRF-3 + alveolar macrophages were observed in COPD and SC compared with nSC subjects. However, in COPD patients, the lower the levels of IRF-3 + alveolar macrophages the lower the FEV1 and the higher the exacerbation rate. The presence of chronic bronchitis (CB) was also associated with low levels of IRF-3 + alveolar macrophages. NKp46 + cells, but not eosinophils, were increased in COPD patients compared to nSC patients (p < 0.0001).

conclusionsSmoking is associated with higher levels of innate immune response as showed by higher levels of IRF-3 + alveolar macrophages and NKp46 + cells. In COPD, exacerbation rates, severe airflow obstruction and CB were associated with lower levels of IRF-3 expression, suggesting that innate immune responses characterize specific clinical traits of the disease.

Indexed as

Interferon Regulatory Factor-3Macrophages, AlveolarPulmonary Disease, Chronic ObstructiveAgedFemaleHumansImmunity, InnateMaleMiddle AgedInterferon Regulatory Factor-3IRF3 protein, humanAirflow limitationChronic bronchitisExacerbationsInnate immunity

Identifiers

PMID39160551
PMCPMC11334339

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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.