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Gene regulation contributes to explain the impact of early life socioeconomic disadvantage on adult inflammatory levels in two cohort studies

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  • معلومة اضافية
    • Contributors:
      Université de Fribourg = University of Fribourg (UNIFR); Université de Lausanne = University of Lausanne (UNIL); Swiss Institute of Bioinformatics Lausanne (SIB); University of Tampere Finland; Epidémiologie et analyses en santé publique : risques, maladies chroniques et handicaps (LEASP); Université Toulouse III - Paul Sabatier (UT3); Université de Toulouse (UT)-Université de Toulouse (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM); Universität Bern / University of Bern (UNIBE); Hôpitaux universitaires de Genève = University Hospitals of Geneva (HUG); University of Turku; Turku University Hospital (TYKS); Imperial College London; University College of London London (UCL); Université de Genève = University of Geneva (UNIGE); Geneva University Hospital (HUG); Tis work was supported by the European Commission grant Horizon 2020 number 633666 and the SwissState Secretariat for Education, Research and Innovation SERI, and by an Ambizione Grant from the SwissNational Science Foundation (PZ00P3_147998).
    • بيانات النشر:
      HAL CCSD
      Nature Publishing Group
    • الموضوع:
      2021
    • Collection:
      Archive ouverte HAL (Hyper Article en Ligne, CCSD - Centre pour la Communication Scientifique Directe)
    • نبذة مختصرة :
      International audience ; Abstract 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.
    • Relation:
      info:eu-repo/semantics/altIdentifier/pmid/33542415; hal-04143232; https://ut3-toulouseinp.hal.science/hal-04143232; https://ut3-toulouseinp.hal.science/hal-04143232/document; https://ut3-toulouseinp.hal.science/hal-04143232/file/CARMELI_2021.pdf; PUBMED: 33542415; PUBMEDCENTRAL: PMC7862626
    • الرقم المعرف:
      10.1038/s41598-021-82714-2
    • Rights:
      http://creativecommons.org/licenses/by/ ; info:eu-repo/semantics/OpenAccess
    • الرقم المعرف:
      edsbas.A5402C1E