Investigating the impact of early-life adversity on physiological, immune, and gene expression responses to acute stress: A pilot feasibility study.
Journal
PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081
Informations de publication
Date de publication:
2020
2020
Historique:
received:
31
07
2019
accepted:
11
03
2020
entrez:
4
4
2020
pubmed:
4
4
2020
medline:
9
7
2020
Statut:
epublish
Résumé
Exposure to early-life adversity (ELA) can result in long-term changes to physiological systems, which predispose individuals to negative health outcomes. This biological embedding of stress-responsive systems may operate via dysregulation of physiological resources in response to common stressors. The present pilot study outlines a novel experimental design to test how young adults' exposure to ELA influences neuroendocrine and inflammatory responses to acute stress. Participants were 12 males (mean age = 21.25), half of whom endorsed at least three significant adverse events up to age 18 years ('ELA group'), and half who confirmed zero ('controls'). Using a randomized within-subjects, between-groups experimental design, we induced acute psychosocial stress (Trier Social Stress Test, TSST), and included a no-stress control condition one week apart. During these sessions, we obtained repeated measurements of physiological reactivity, gene expression of the glucocorticoid receptor (NR3C1), and plasma levels of pro-inflammatory cytokines (IL-1β, IL-6, IL-8 and TNFα) over a 4-hour window post-test. In this pilot study, the ELA group evinced higher cortisol response and blunted NR3C1 gene expression in response to the TSST compared with controls, while no differences were observed in the no-stress condition. For pro-inflammatory cytokines, only IL-6 increased significantly in response to the TSST, with no differences between the two groups. Overall, this pilot feasibility study provides a framework to investigate the biological embedding of early-adversity via dysregulation across physiological and genomic systems in response to acute psychosocial stress. ELA may program such systems in a maladaptive manner more likely to manifest during times of duress, predisposing individuals to the negative health consequences of everyday stressors. Future studies with larger sample size including both males and females are needed to replicate and expand upon these preliminary findings.
Identifiants
pubmed: 32243432
doi: 10.1371/journal.pone.0221310
pii: PONE-D-19-21614
pmc: PMC7122782
doi:
Substances chimiques
Cytokines
0
NR3C1 protein, human
0
Receptors, Glucocorticoid
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
e0221310Subventions
Organisme : NIA NIH HHS
ID : R21 AG054846
Pays : United States
Organisme : NIA NIH HHS
ID : R21 AG055621
Pays : United States
Organisme : NIA NIH HHS
ID : T32 AG049676
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR002014
Pays : United States
Déclaration de conflit d'intérêts
The authors have declared that no competing interests exist.
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