Neuroimmunoendocrine Interactions in Post-Traumatic Stress Disorder: Focus on Long-Term Implications of Childhood Maltreatment
| Autor: | Andrea Wieck, Antônio Lúcio Teixeira, Carine Hartmann do Prado, Moisés Evandro Bauer, Rodrigo Grassi-Oliveira |
|---|---|
| Rok vydání: | 2014 |
| Předmět: |
Child abuse
medicine.medical_specialty Neuroimmunomodulation Immunology Inflammation Stress Disorders Post-Traumatic Endocrinology Immune system Immunity medicine Animals Humans Child Abuse Child Psychiatry Depression (differential diagnoses) Endocrine and Autonomic Systems Adult Survivors of Child Abuse Traumatic stress Neurosecretory Systems Hypercortisolemia Neurology medicine.symptom Psychology Stress Psychological Glucocorticoid medicine.drug |
| Zdroj: | Neuroimmunomodulation. 21:145-151 |
| ISSN: | 1423-0216 1021-7401 |
| DOI: | 10.1159/000356552 |
| Popis: | Childhood maltreatment has been linked to enhanced vulnerability to psychiatric pathologies in adult life, including post-traumatic stress disorder (PTSD). Previous works have reported cogent neuroendocrine and immune changes related to adult traumatic events (war survivors, refugees, etc.), but little information is known regarding the impact of early-life stress (ELS) in adult physiology. Here, we review the neuroendocrine and immunological changes commonly observed in PTSD, focusing on the long-term implications of ELS. Childhood maltreatment may lead to altered glucocorticoid (GC) secretion, resulting in hypo- or hypercortisolemia, and reciprocal changes in peripheral leukocyte sensitivity to GC. It is believed that these neuroendocrine changes are correlated with the immune imbalance phenomenon (low-grade inflammation), characterized by increased plasma levels of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) and C-reactive protein. Changes in peripheral lymphocyte subsets are also documented, such as a reduction in regulatory T cells and an expansion of activated T cells. The excess of circulating cytokines may thus interfere with key brain neurotransmitter pathways involved in depression and enhanced risk to cardiovascular, respiratory, gastrointestinal, inflammatory and autoimmune diseases. Recent gene-environment and epigenetic findings have indicated potential molecular mechanisms linking ELS, neuroendocrine and immunity in PTSD. |
| Databáze: | OpenAIRE |
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