Journal
SCIENTIFIC REPORTS
Volume 11, Issue 1, Pages -Publisher
NATURE PORTFOLIO
DOI: 10.1038/s41598-021-82714-2
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Funding
- European Commission [633666]
- Swiss State Secretariat for Education, Research and Innovation SERI
- Swiss National Science Foundation [31003A_169929, PZ00P3_147998, 33CM30-124087]
- Academy of Finland [322098, 286284, 134309, 126925, 121584, 124282, 129378, 117787, 41071, 311492]
- Social Insurance Institution of Finland
- Competitive State Research Financing of the Expert Responsibility area of Kuopio, Tampere and Turku University Hospitals [X51001]
- Juho Vainio Foundation
- Paavo Nurmi Foundation
- Finnish Foundation for Cardiovascular Research
- Finnish Cultural Foundation
- Sigrid Juselius Foundation
- Tampere Tuberculosis Foundation
- Emil Aaltonen Foundation
- Yrjo Jahnsson Foundation
- Diabetes Research Foundation of Finnish Diabetes Association
- EU [755320]
- European Research Council [742927]
- Tampere University Hospital Supporting Foundation
- UK Medical Research Council [R024227, S011676]
- US National Institute on Aging (NIH) [R01AG056477]
- NordForsk
- MRC [MR/S011676/1, MR/S019669/1, MR/R024227/1] Funding Source: UKRI
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Research indicates that individuals who experienced socioeconomic disadvantage in childhood are more likely to develop inflammation-related diseases later in life. The study suggests that transcriptional activity plays a significant role in mediating the effect of early life social exposures on adulthood inflammation levels. Additionally, the findings highlight that mechanisms other than cis DNA methylation may contribute to regulating transcriptional fingerprints.
Individuals experiencing socioeconomic disadvantage in childhood have a higher rate of inflammation-related diseases decades later. Little is known about the mechanisms linking early life experiences to the functioning of the immune system in adulthood. To address this, we explore the relationship across social-to-biological layers of early life social exposures on levels of adulthood inflammation and the mediating role of gene regulatory mechanisms, epigenetic and transcriptomic profiling from blood, in 2,329 individuals from two European cohort studies. Consistently across both studies, we find transcriptional activity explains a substantive proportion (78% and 26%) of the estimated effect of early life disadvantaged social exposures on levels of adulthood inflammation. Furthermore, we show that mechanisms other than cis DNA methylation may regulate those transcriptional fingerprints. These results further our understanding of social-to-biological transitions by pinpointing the role of gene regulation that cannot fully be explained by differential cis DNA methylation.
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