Citation

Witek Janusek L, Tell D, Gaylord-Harden N, Mathews HL. Brain Behav. Immun. 2016; 60: 126-135.

Affiliation

Department of Microbiology and Immunology, Stritch School of Medicine, Loyola University Chicago, Health Science Division, 2160 South First Ave., Maywood, IL 60153.

Copyright

(Copyright © 2016, Elsevier Publishing)

DOI

10.1016/j.bbi.2016.10.006

PMID

27765646

Abstract

African American men (AAM) who are exposed to trauma and adversity during their early life are at greater risk for poor health over their lifespan. Exposure to adversity during critical developmental windows may embed an epigenetic signature that alters expression of genes that regulate stress response systems, including those genes that regulate the inflammatory response to stress. Such an epigenetic signature may increase risk for diseases exacerbated by inflammation, and may contribute to health disparity. The purpose of this study was to evaluate the extent to which exposure to early life adversity influences the psychological, cortisol, and proinflammatory response to acute stress (Trier Social Stress Test - TSST) in emerging adult AAM, ages 18-25 years (N= 34). Hierarchical linear modeling was used to examine the cortisol and IL-6 pattern of response to the TSST with respect to childhood adversity factors and DNA methylation of the IL-6 promoter.

FINDINGS revealed that in response to the TSST, greater levels of childhood trauma and indirect exposure to neighborhood violence were associated with a greater TSST-induced IL-6 response, and a blunted cortisol response. Reduced methylation of the IL6 promoter was related to increased exposure to childhood trauma and greater TSST-induced IL-6 levels. These results support the concept that exposure to childhood adversity amplifies the adult proinflammatory response to stress, which is related to epigenetic signature.

Copyright © 2016. Published by Elsevier Inc.

Language: en