Major stress in early childhood strengthens the association between peripheral inflammatory activity and corticostriatal responsivity to reward.

Autor: Miller GE; Institute for Policy Research, Northwestern University, United States; Department of Psychology, Northwestern University, United States. Electronic address: greg.miller@northwestern.edu., Carroll AL; Institute for Policy Research, Northwestern University, United States., Armstrong CC; Institute for Policy Research, Northwestern University, United States., Craske MG; Department of Psychology, University of California, Los Angeles, United States., Zinbarg RE; Institute for Policy Research, Northwestern University, United States; The Family Institute at Northwestern University, United States., Bookheimer SY; Department of Psychology, University of California, Los Angeles, United States., Ka-Yi Chat I; Department of Psychology & Neuroscience, Temple University, United States., Vinograd M; Department of Psychology, University of California, Los Angeles, United States., Young KS; Department of Psychology, University of California, Los Angeles, United States., Nusslock R; Institute for Policy Research, Northwestern University, United States; Department of Psychology, Northwestern University, United States.
Jazyk: angličtina
Zdroj: Brain, behavior, and immunity [Brain Behav Immun] 2024 Mar; Vol. 117, pp. 215-223. Date of Electronic Publication: 2024 Jan 19.
DOI: 10.1016/j.bbi.2024.01.013
Abstrakt: Background: Severe, chronic stress during childhood accentuates vulnerability to mental and physical health problems across the lifespan. To explain this phenomenon, the neuroimmune network hypothesis proposes that childhood stressors amplify signaling between peripheral inflammatory cells and developing brain circuits that support processing of rewards and threats. Here, we conducted a preliminary test of the basic premises of this hypothesis.
Methods: 180 adolescents (mean age = 19.1 years; 68.9 % female) with diverse racial and ethnic identities (56.1 % White; 28.3 % Hispanic; 26.1 % Asian) participated. The Childhood Trauma Interview was administered to quantify early adversity. Five inflammatory biomarkers were assayed in antecubital blood - C-reactive protein, tumor necrosis factor-a, and interleukins-6, -8, and -10 - and were averaged to form a composite score. Participants also completed a functional MRI task to measure corticostriatal responsivity to the anticipation and acquisition of monetary rewards.
Results: Stress exposure and corticostriatal responsivity interacted statistically to predict the inflammation composite. Among participants who experienced major stressors in the first decade of life, higher inflammatory activity covaried with lower corticostriatal responsivity during acquisition of monetary rewards. This relationship was specific to participants who experienced major stress in early childhood, implying a sensitive period for exposure, and were evident in both the orbitofrontal cortex and the ventral striatum, suggesting the broad involvement of corticostriatal regions. The findings were independent of participants' age, sex, racial and ethnic identity, family income, and depressive symptoms.
Conclusions: Collectively, the results are consistent with hypotheses suggesting that major stress in childhood alters brain-immune signaling.
Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2024 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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