A Brief Historic Review of Research on Early Life Stress and Inflammation across the Lifespan

被引:0
|
作者
Entringer, Sonja [1 ,2 ,3 ,4 ,5 ]
Heim, Christine [1 ,2 ,3 ,5 ,6 ]
机构
[1] Charite Univ Med Berlin, Berlin, Germany
[2] Humboldt Univ, Berlin, Germany
[3] Inst Med Psychol, Berlin, Germany
[4] Univ Calif Irvine, Dept Pediat, Irvine, CA 92697 USA
[5] German Ctr Mental Hlth, Berlin, Germany
[6] NeuroCure Cluster Excellence, Berlin, Germany
关键词
Stress; Development; Immune system; Inflammation; Disease risk; ADVERSE CHILDHOOD EXPERIENCES; C-REACTIVE PROTEIN; SHORTER TELOMERE LENGTH; PRENATAL STRESS; PSYCHOSOCIAL STRESS; CYTOKINE PRODUCTION; MAJOR DEPRESSION; MATERNAL STRESS; IMMUNE MEASURES; SEX-DIFFERENCES;
D O I
10.1159/000542676
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background: Extensive evidence from animal and human studies indicates that exposure to stress during sensitive developmental periods significantly increases the risk for psychiatric and physical disorders, resulting in reduced longevity. Chronic immune activation has been suggested as one pathway through which early adverse experiences may become biologically embedded. This paper highlights selected key findings and questions that first emerged in the literature and founded the field and then examines how research methods and questions have evolved over time. Summary: During the past decades, evidence from preclinical, clinical, and epidemiological studies has accumulated suggesting consequences of early life stress (ELS) exposure for immune function, particularly increased chronic inflammation or inflammatory responses. Scientific approaches to study the effects of ELS on the immune system have changed since the first studies on this topic were published. Key Messages: Across different study designs, species, and methods, a consistent association between childhood adversity and a pro-inflammatory phenotype has been reported. We critically discuss which topics warrant further consideration and how current findings could be used to develop targeted interventions to prevent or reverse the biological embedding of ELS and resultant disease manifestations.
引用
收藏
页码:24 / 35
页数:12
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