Oxidative stress and Nrf2 expression in peripheral blood mononuclear cells derived from COPD patients: an observational longitudinal study.


Journal

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

Informations de publication

Date de publication:
30 Jan 2020
Historique:
received: 21 08 2019
accepted: 14 01 2020
entrez: 1 2 2020
pubmed: 1 2 2020
medline: 24 11 2020
Statut: epublish

Résumé

A persistent low inflammatory-oxidative status and the inadequacy of the antioxidant nuclear factor-E2-related factor 2 (Nrf2) have been implicated in chronic obstructive pulmonary disease (COPD) progression. Therefore this study was aimed to assess the association between lung function decline and oxidative-inflammatory markers and Nrf2 signaling pathway expression in peripheral blood mononuclear cells (PBMCs) over time. 33 mild-moderate COPD outpatients (mean age 66.9 ± 6.9 years) were age-sex matched with 37 no-COPD subjects. A clinical evaluation, blood sampling tests and a spirometry were performed at baseline and after a mean follow-up of 49.7 ± 6.9 months. In COPD, compared to no-COPD, we found a faster lung function decline at follow-up. Although similar prevalence of smoking, hypertension, diabetes and dyslipidemia, systemic markers of inflammation (hs-CRP and white blood cells, WBCs) and oxidative stress (8-isoprostane) were significantly increased in COPD at follow-up, while the antioxidant glutathione (GSH) was significantly reduced. Moreover the expression of Nrf2 and of Nrf2-related genes heme oxygenase (HO)-1 and glutamate-cysteine ligase catalytic (GCLC) subunit in PBMCS were significantly down-regulated in COPD at follow-up, whereas no changes were observed in no-COPD. The percent variation (Δ) of FEV Although our results must be confirmed in larger trial they suggest that the down-regulation of Nrf2/ARE gene expression in PBMCs may be one of the determinants of FEV

Sections du résumé

BACKGROUND BACKGROUND
A persistent low inflammatory-oxidative status and the inadequacy of the antioxidant nuclear factor-E2-related factor 2 (Nrf2) have been implicated in chronic obstructive pulmonary disease (COPD) progression. Therefore this study was aimed to assess the association between lung function decline and oxidative-inflammatory markers and Nrf2 signaling pathway expression in peripheral blood mononuclear cells (PBMCs) over time.
METHODS METHODS
33 mild-moderate COPD outpatients (mean age 66.9 ± 6.9 years) were age-sex matched with 37 no-COPD subjects. A clinical evaluation, blood sampling tests and a spirometry were performed at baseline and after a mean follow-up of 49.7 ± 6.9 months.
RESULTS RESULTS
In COPD, compared to no-COPD, we found a faster lung function decline at follow-up. Although similar prevalence of smoking, hypertension, diabetes and dyslipidemia, systemic markers of inflammation (hs-CRP and white blood cells, WBCs) and oxidative stress (8-isoprostane) were significantly increased in COPD at follow-up, while the antioxidant glutathione (GSH) was significantly reduced. Moreover the expression of Nrf2 and of Nrf2-related genes heme oxygenase (HO)-1 and glutamate-cysteine ligase catalytic (GCLC) subunit in PBMCS were significantly down-regulated in COPD at follow-up, whereas no changes were observed in no-COPD. The percent variation (Δ) of FEV
CONCLUSIONS CONCLUSIONS
Although our results must be confirmed in larger trial they suggest that the down-regulation of Nrf2/ARE gene expression in PBMCs may be one of the determinants of FEV

Identifiants

pubmed: 32000766
doi: 10.1186/s12931-020-1292-7
pii: 10.1186/s12931-020-1292-7
pmc: PMC6993453
doi:

Substances chimiques

NF-E2-Related Factor 2 0
NFE2L2 protein, human 0

Types de publication

Journal Article Observational Study

Langues

eng

Sous-ensembles de citation

IM

Pagination

37

Commentaires et corrections

Type : ErratumIn

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Auteurs

A M Fratta Pasini (AM)

Department of Medicine, Section of General Medicine and Atherothrombotic and Degenerative Diseases, University of Verona, Verona, Italy. annamaria.frattapasini@univr.it.

C Stranieri (C)

Department of Medicine, Section of General Medicine and Atherothrombotic and Degenerative Diseases, University of Verona, Verona, Italy.

M Ferrari (M)

Department of Medicine, Unit of Respiratory Diseases, Verona, Italy.

U Garbin (U)

Department of Medicine, Section of General Medicine and Atherothrombotic and Degenerative Diseases, University of Verona, Verona, Italy.

L Cazzoletti (L)

Department of Diagnostics and Public Health, Unit of Epidemiology & Medical Statistics, University of Verona, Verona, Italy.

C Mozzini (C)

Department of Medicine, Section of General Medicine and Atherothrombotic and Degenerative Diseases, University of Verona, Verona, Italy.

F Spelta (F)

Department of Medicine, Section of General Medicine and Atherothrombotic and Degenerative Diseases, University of Verona, Verona, Italy.

D Peserico (D)

Department of Medicine, Section of General Medicine and Atherothrombotic and Degenerative Diseases, University of Verona, Verona, Italy.

L Cominacini (L)

Department of Medicine, Section of General Medicine and Atherothrombotic and Degenerative Diseases, University of Verona, Verona, Italy.

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