Plasma metabolomics and quantitative interstitial abnormalities in ever-smokers.

Humans Smokers Niacin Lung Pulmonary Emphysema / diagnostic imaging Emphysema Niacinamide Pulmonary Disease, Chronic Obstructive / diagnostic imaging
Cross-Sectional Studies Lung Diseases, Interstitial Metabolomics Pulmonary Emphysema Tomography, X-Ray Computed

Journal

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

Informations de publication

Date de publication:
04 Nov 2023
Historique:
received: 12 09 2023
accepted: 23 10 2023
medline: 6 11 2023
pubmed: 5 11 2023
entrez: 5 11 2023
Statut: epublish

Résumé

Quantitative interstitial abnormalities (QIA) are an automated computed tomography (CT) finding of early parenchymal lung disease, associated with worse lung function, reduced exercise capacity, increased respiratory symptoms, and death. The metabolomic perturbations associated with QIA are not well known. We sought to identify plasma metabolites associated with QIA in smokers. We also sought to identify shared and differentiating metabolomics features between QIA and emphysema, another smoking-related advanced radiographic abnormality. In 928 former and current smokers in the Genetic Epidemiology of COPD cohort, we measured QIA and emphysema using an automated local density histogram method and generated metabolite profiles from plasma samples using liquid chromatography-mass spectrometry (Metabolon). We assessed the associations between metabolite levels and QIA using multivariable linear regression models adjusted for age, sex, body mass index, smoking status, pack-years, and inhaled corticosteroid use, at a Benjamini-Hochberg False Discovery Rate p-value of ≤ 0.05. Using multinomial regression models adjusted for these covariates, we assessed the associations between metabolite levels and the following CT phenotypes: QIA-predominant, emphysema-predominant, combined-predominant, and neither- predominant. Pathway enrichment analyses were performed using MetaboAnalyst. We found 85 metabolites significantly associated with QIA, with overrepresentation of the nicotinate and nicotinamide, histidine, starch and sucrose, pyrimidine, phosphatidylcholine, lysophospholipid, and sphingomyelin pathways. These included metabolites involved in inflammation and immune response, extracellular matrix remodeling, surfactant, and muscle cachexia. There were 75 metabolites significantly different between QIA-predominant and emphysema-predominant phenotypes, with overrepresentation of the phosphatidylethanolamine, nicotinate and nicotinamide, aminoacyl-tRNA, arginine, proline, alanine, aspartate, and glutamate pathways. Metabolomic correlates may lend insight to the biologic perturbations and pathways that underlie clinically meaningful quantitative CT measurements like QIA in smokers.

Sections du résumé

BACKGROUND BACKGROUND
Quantitative interstitial abnormalities (QIA) are an automated computed tomography (CT) finding of early parenchymal lung disease, associated with worse lung function, reduced exercise capacity, increased respiratory symptoms, and death. The metabolomic perturbations associated with QIA are not well known. We sought to identify plasma metabolites associated with QIA in smokers. We also sought to identify shared and differentiating metabolomics features between QIA and emphysema, another smoking-related advanced radiographic abnormality.
METHODS METHODS
In 928 former and current smokers in the Genetic Epidemiology of COPD cohort, we measured QIA and emphysema using an automated local density histogram method and generated metabolite profiles from plasma samples using liquid chromatography-mass spectrometry (Metabolon). We assessed the associations between metabolite levels and QIA using multivariable linear regression models adjusted for age, sex, body mass index, smoking status, pack-years, and inhaled corticosteroid use, at a Benjamini-Hochberg False Discovery Rate p-value of ≤ 0.05. Using multinomial regression models adjusted for these covariates, we assessed the associations between metabolite levels and the following CT phenotypes: QIA-predominant, emphysema-predominant, combined-predominant, and neither- predominant. Pathway enrichment analyses were performed using MetaboAnalyst.
RESULTS RESULTS
We found 85 metabolites significantly associated with QIA, with overrepresentation of the nicotinate and nicotinamide, histidine, starch and sucrose, pyrimidine, phosphatidylcholine, lysophospholipid, and sphingomyelin pathways. These included metabolites involved in inflammation and immune response, extracellular matrix remodeling, surfactant, and muscle cachexia. There were 75 metabolites significantly different between QIA-predominant and emphysema-predominant phenotypes, with overrepresentation of the phosphatidylethanolamine, nicotinate and nicotinamide, aminoacyl-tRNA, arginine, proline, alanine, aspartate, and glutamate pathways.
CONCLUSIONS CONCLUSIONS
Metabolomic correlates may lend insight to the biologic perturbations and pathways that underlie clinically meaningful quantitative CT measurements like QIA in smokers.

Identifiants

DOI: 10.1186/s12931-023-02576-2 PMID: 37925418 PMC: PMC10625195
pubmed: 37925418
doi: 10.1186/s12931-023-02576-2
pii: 10.1186/s12931-023-02576-2
pmc: PMC10625195
doi:

Substances chimiques

Niacin 2679MF687A
Niacinamide 25X51I8RD4

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

265

Informations de copyright

© 2023. The Author(s).

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Auteurs

Bina Choi (B)

Division of Pulmonary and Critical Care Medicine, Department of Medicine, Brigham and Women's Hospital, 75 Francis Street, Pulmonary-PBB-CA-3, Boston, MA, 02115, USA. bchoi4@bwh.harvard.edu.
Applied Chest Imaging Laboratory, Brigham and Women's Hospital, Boston, MA, USA. bchoi4@bwh.harvard.edu.

Raúl San José Estépar (R)

Applied Chest Imaging Laboratory, Brigham and Women's Hospital, Boston, MA, USA.
Department of Radiology, Brigham and Women's Hospital, Boston, MA, USA.

Suneeta Godbole (S)

Anschutz Medical Campus, Department of Biostatistics and Informatics, University of Colorado, Aurora, CO, USA.

Jeffrey L Curtis (JL)

Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA.
Medical Service, VA Ann Arbor Healthcare System, Ann Arbor, MI, USA.

Jennifer M Wang (JM)

Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA.

Rubén San José Estépar (R)

Applied Chest Imaging Laboratory, Brigham and Women's Hospital, Boston, MA, USA.
Department of Radiology, Brigham and Women's Hospital, Boston, MA, USA.

Ivan O Rosas (IO)

Baylor College of Medicine, Houston, TX, USA.

Jared R Mayers (JR)

Division of Pulmonary and Critical Care Medicine, Department of Medicine, Brigham and Women's Hospital, 75 Francis Street, Pulmonary-PBB-CA-3, Boston, MA, 02115, USA.

Brian D Hobbs (BD)

Division of Pulmonary and Critical Care Medicine, Department of Medicine, Brigham and Women's Hospital, 75 Francis Street, Pulmonary-PBB-CA-3, Boston, MA, 02115, USA.
Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA.

Craig P Hersh (CP)

Division of Pulmonary and Critical Care Medicine, Department of Medicine, Brigham and Women's Hospital, 75 Francis Street, Pulmonary-PBB-CA-3, Boston, MA, 02115, USA.
Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA.

Samuel Y Ash (SY)

Applied Chest Imaging Laboratory, Brigham and Women's Hospital, Boston, MA, USA.
Department of Critical Care, South Shore Hospital, South Weymouth, MA, USA.

MeiLan K Han (MK)

Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA.

Russell P Bowler (RP)

Division of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, National Jewish Health, Denver, CO, USA.

Kathleen A Stringer (KA)

Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA.
Department of Clinical Pharmacy, College of Pharmacy, University of Michigan, Ann Arbor, MI, USA.

George R Washko (GR)

Division of Pulmonary and Critical Care Medicine, Department of Medicine, Brigham and Women's Hospital, 75 Francis Street, Pulmonary-PBB-CA-3, Boston, MA, 02115, USA.
Applied Chest Imaging Laboratory, Brigham and Women's Hospital, Boston, MA, USA.

Wassim W Labaki (WW)

Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA.

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questionsmedicales.fr › Personnes › Fumeurs › Plasma metabolomics and quantitative...
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questionsmedicales.fr › Appareil respiratoire › Poumon › Plasma metabolomics and quantitative...
questionsmedicales.fr › États, signes et symptômes pathologiques › Processus pathologiques › Caractéristiques de la maladie › Maladie chronique › Broncho-pneumopathie chronique obstructive › Emphysème pulmonaire › Plasma metabolomics and quantitative...
questionsmedicales.fr › États, signes et symptômes pathologiques › Processus pathologiques › Emphysème › Plasma metabolomics and quantitative...
questionsmedicales.fr › Composés hétérocycliques › Composés hétéromonocycliques › Pyridines › Acides nicotiniques › Nicotinamide › Plasma metabolomics and quantitative...
questionsmedicales.fr › États, signes et symptômes pathologiques › Processus pathologiques › Caractéristiques de la maladie › Maladie chronique › Broncho-pneumopathie chronique obstructive › Plasma metabolomics and quantitative...