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


Journal

Respiratory research
ISSN: 1465-993X
Titre abrégé: Respir Res
Pays: England
ID NLM: 101090633

Informations de publication

Date de publication:
19 Aug 2024
Historique:
received: 19 12 2023
accepted: 13 08 2024
medline: 20 8 2024
pubmed: 20 8 2024
entrez: 19 8 2024
Statut: epublish

Résumé

Chronic 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. To 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. Lung 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. A 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). Smoking 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.

Identifiants

pubmed: 39160551
doi: 10.1186/s12931-024-02952-6
pii: 10.1186/s12931-024-02952-6
doi:

Substances chimiques

Interferon Regulatory Factor-3 0
IRF3 protein, human 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

315

Informations de copyright

© 2024. The Author(s).

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Auteurs

Simonetta Baraldo (S)

Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padova, Padova, Italy.

Matteo Bonato (M)

Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padova, Padova, Italy.
Pulmonology Unit, Ca' Foncello Hospital, Azienda Unità Locale Socio-Sanitaria 2 Marca Trevigiana, Treviso, Italy.

Sebastiano Cassia (S)

Respiratory Clinic, Department of Internal Medicine, University of Genoa, Genoa, Italy.
IRCCS Ospedale Policlinico San Martino, Genoa, Italy.

Paolo Casolari (P)

Section of Respiratory Diseases, Department of Translational Medicine, University of Ferrara, Ferrara, Italy.

Laura De Ferrari (L)

Respiratory Clinic, Department of Internal Medicine, University of Genoa, Genoa, Italy.
IRCCS Ospedale Policlinico San Martino, Genoa, Italy.

Mariaenrica Tiné (M)

Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padova, Padova, Italy.

Federico Baraldi (F)

Section of Respiratory Diseases, Department of Translational Medicine, University of Ferrara, Ferrara, Italy.

Tommaso Bigoni (T)

Section of Respiratory Diseases, Department of Translational Medicine, University of Ferrara, Ferrara, Italy.

Anna Maria Riccio (AM)

Respiratory Clinic, Department of Internal Medicine, University of Genoa, Genoa, Italy.
IRCCS Ospedale Policlinico San Martino, Genoa, Italy.

Fulvio Braido (F)

Respiratory Clinic, Department of Internal Medicine, University of Genoa, Genoa, Italy.
IRCCS Ospedale Policlinico San Martino, Genoa, Italy.

Marina Saetta (M)

Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padova, Padova, Italy.

Alberto Papi (A)

Section of Respiratory Diseases, Department of Translational Medicine, University of Ferrara, Ferrara, Italy.
Azienda Ospedaliera Universitaria Ferrara and AUSL, Ferrara, Italy.

Marco Contoli (M)

Section of Respiratory Diseases, Department of Translational Medicine, University of Ferrara, Ferrara, Italy. ctm@unife.it.
Azienda Ospedaliera Universitaria Ferrara and AUSL, Ferrara, Italy. ctm@unife.it.

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