Abstract
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.
| Original language | English |
|---|---|
| Pages (from-to) | 1320-1330 |
| Number of pages | 11 |
| Journal | International Journal of Epidemiology |
| Volume | 44 |
| Issue number | 4 |
| DOIs | |
| Publication status | Published - Aug 1 2015 |
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Keywords
- DNA methylation
- Inflammation
- Life course
- Socioeconomic status
ASJC Scopus subject areas
- Epidemiology
Cite this
Life-course socioeconomic status and DNA methylation of genes regulating inflammation. / Stringhini, Silvia; Polidoro, Silvia; Sacerdote, Carlotta; Kelly, Rachel S.; Van Veldhoven, Karin; Agnoli, Claudia; Grioni, Sara; Tumino, Rosario; Giurdanella, Maria Concetta; Panico, Salvatore; Mattiello, Amalia; Palli, Domenico; Masala, Giovanna; Gallo, Valentina; Castagné, Raphaële; Paccaud, Fred; Campanella, Gianluca; Chadeau-Hyam, Marc; Vineis, Paolo.
In: International Journal of Epidemiology, Vol. 44, No. 4, 01.08.2015, p. 1320-1330.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Life-course socioeconomic status and DNA methylation of genes regulating inflammation
AU - Stringhini, Silvia
AU - Polidoro, Silvia
AU - Sacerdote, Carlotta
AU - Kelly, Rachel S.
AU - Van Veldhoven, Karin
AU - Agnoli, Claudia
AU - Grioni, Sara
AU - Tumino, Rosario
AU - Giurdanella, Maria Concetta
AU - Panico, Salvatore
AU - Mattiello, Amalia
AU - Palli, Domenico
AU - Masala, Giovanna
AU - Gallo, Valentina
AU - Castagné, Raphaële
AU - Paccaud, Fred
AU - Campanella, Gianluca
AU - Chadeau-Hyam, Marc
AU - Vineis, Paolo
PY - 2015/8/1
Y1 - 2015/8/1
N2 - 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.
AB - 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.
KW - DNA methylation
KW - Inflammation
KW - Life course
KW - Socioeconomic status
UR - http://www.scopus.com/inward/record.url?scp=84943776956&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84943776956&partnerID=8YFLogxK
U2 - 10.1093/ije/dyv060
DO - 10.1093/ije/dyv060
M3 - Article
C2 - 25889032
AN - SCOPUS:84943776956
VL - 44
SP - 1320
EP - 1330
JO - International Journal of Epidemiology
JF - International Journal of Epidemiology
SN - 0300-5771
IS - 4
ER -