Background: Childhood maltreatment confers higher risk of adulthood mental disease. However, the biological mechanism mediating this association remains largely unknown, with evidence suggesting dysregulation of the immune system as a possible biological mediator. The present paper conducted a case-control study to establish whether early-life adversity contributes to potentially pathogenic pro-inflammatory phenotypes in adult Panic Disorder (PD) individuals.
Methods: Eighty-four PD patients and seventy-eight matched healthy controls were assessed for peripheral serum levels of interleukin (IL)-2R, IL-1β, IL-10, and for specific trauma types through child trauma questionnaire evaluation.
Results: Analyses for specific types of trauma (sexual, physical or emotional abuse or neglect) revealed that these impact differentially the single inflammatory markers, and a significant association between physical abuse and the inflammatory marker IL-2R in PD patients was observed (β = 0.40, p = 0.013). The analysis demonstrates that childhood trauma contributes to a proinflammatory state in adulthood, with specific inflammatory profiles counting on the specific type of traumatic event.
Conclusion: This study is unique in providing inflammatory biomarkers evidence of distinct biological modifications in PD in the presence or absence of exposure to childhood abuse. These results contribute to a better understanding of the extent of influence of differences in trauma exposure on pathophysiological processes in PD and may have implications for personalized medicine.
Keywords: Anxiety; Early life stress; Immunology; Neurodevelopment.
Copyright © 2021. Published by Elsevier B.V.