Fiche du document
2015
- doi: 10.1093/ije/dyv060
- issn: 0300-5771
Ce document est lié à :
info:eu-repo/semantics/altIdentifier/doi/10.1093/ije/dyv060
Ce document est lié à :
info:eu-repo/semantics/altIdentifier/pmid/25889032
Ce document est lié à :
info:eu-repo/semantics/altIdentifier/eissn/1464-3685
Ce document est lié à :
info:eu-repo/semantics/altIdentifier/urn/urn:nbn:ch:serval-BIB_F12A1F4CB65A9
info:eu-repo/semantics/openAccess , Copying allowed only for non-profit organizations , https://serval.unil.ch/disclaimer
Sujets proches
Units of inheritance Units of heredityCiter ce document
S. Stringhini et al., « Life-course socioeconomic status and DNA methylation of genes regulating inflammation », Serveur académique Lausannois, ID : 10.1093/ije/dyv060
Métriques
Partage / Export
Résumé
BACKGROUND: In humans, low socioeconomic status (SES) across the life course is associated with greater diurnal cortisol production, increased inflammatory activity and higher circulating antibodies for several pathogens, all suggesting a dampened immune response. Recent evidence suggests that DNA methylation of pro-inflammatory genes may be implicated in the biological embedding of the social environment. METHODS: The present study examines the association between life-course SES and DNA methylation of candidate genes, selected on the basis of their involvement in SES-related inflammation, in the context of a genome-wide methylation study. Participants were 857 healthy individuals sampled from the EPIC Italy prospective cohort study. RESULTS: Indicators of SES were associated with DNA methylation of genes involved in inflammation. NFATC1, in particular, was consistently found to be less methylated in individuals with low vs high SES, in a dose-dependent manner. IL1A, GPR132 and genes belonging to the MAPK family were also less methylated among individuals with low SES. In addition, associations were found between SES and CXCL2 and PTGS2, but these genes were consistently more methylated among low SES individuals. CONCLUSIONS: Our findings support the hypothesis that the social environment leaves an epigenetic signature in cells. Although the functional significance of SES-related DNA methylation is still unclear, we hypothesize that it may link SES to chronic disease risk.