Smoking affects epigenetic ageing of lung bronchoalveolar lavage cells in Multiple Sclerosis.
Ageing
DNA methylation
Epigenetic clocks
Inflammation
Lung alveolar macrophages
Multiple Sclerosis
Smoking
Journal
Multiple sclerosis and related disorders
ISSN: 2211-0356
Titre abrégé: Mult Scler Relat Disord
Pays: Netherlands
ID NLM: 101580247
Informations de publication
Date de publication:
Nov 2023
Nov 2023
Historique:
received:
28
04
2023
revised:
18
06
2023
accepted:
02
09
2023
medline:
10
11
2023
pubmed:
15
9
2023
entrez:
14
9
2023
Statut:
ppublish
Résumé
A compelling body of evidence implicates cigarette smoking and lung inflammation in Multiple Sclerosis (MS) susceptibility and progression. Previous studies have reported epigenetic age (DNAm age) acceleration in blood immune cells and in glial cells of people with MS (pwMS) compared to healthy controls (HC). We aimed to examine biological ageing in lung immune cells in the context of MS and smoking. We analyzed age acceleration residuals in lung bronchoalveolar lavage (BAL) cells, constituted of mainly alveolar macrophages, from 17 pwMS and 22 HC in relation to smoking using eight DNA methylation-based clocks, namely AltumAge, Horvath, GrimAge, PhenoAge, Zhang, SkinBlood, Hannum, Monocyte clock as well as two RNA-based clocks, which capture different aspects of biological ageing. After adjustment for covariates, five epigenetic clocks showed significant differences between the groups. Four of them, Horvath (P BAL cells of pwMS display inflammation-related and smoking-dependent changes associated to epigenetic ageing captured by the AltumAge clock. Future studies examining potential confounders, such as the distribution of distinct BAL myeloid cell types in pwMS compared to control individuals in relation to smoking may clarify the varying performance and DNAm age estimations among epigenetic clocks.
Sections du résumé
BACKGROUND
BACKGROUND
A compelling body of evidence implicates cigarette smoking and lung inflammation in Multiple Sclerosis (MS) susceptibility and progression. Previous studies have reported epigenetic age (DNAm age) acceleration in blood immune cells and in glial cells of people with MS (pwMS) compared to healthy controls (HC).
OBJECTIVES
OBJECTIVE
We aimed to examine biological ageing in lung immune cells in the context of MS and smoking.
METHODS
METHODS
We analyzed age acceleration residuals in lung bronchoalveolar lavage (BAL) cells, constituted of mainly alveolar macrophages, from 17 pwMS and 22 HC in relation to smoking using eight DNA methylation-based clocks, namely AltumAge, Horvath, GrimAge, PhenoAge, Zhang, SkinBlood, Hannum, Monocyte clock as well as two RNA-based clocks, which capture different aspects of biological ageing.
RESULTS
RESULTS
After adjustment for covariates, five epigenetic clocks showed significant differences between the groups. Four of them, Horvath (P
CONCLUSIONS
CONCLUSIONS
BAL cells of pwMS display inflammation-related and smoking-dependent changes associated to epigenetic ageing captured by the AltumAge clock. Future studies examining potential confounders, such as the distribution of distinct BAL myeloid cell types in pwMS compared to control individuals in relation to smoking may clarify the varying performance and DNAm age estimations among epigenetic clocks.
Identifiants
pubmed: 37708820
pii: S2211-0348(23)00492-3
doi: 10.1016/j.msard.2023.104991
pii:
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
104991Informations de copyright
Copyright © 2023 The Author(s). Published by Elsevier B.V. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of Competing Interest Authors declare that they have no conflict of interest.