期刊
BIOLOGICAL PSYCHIATRY
卷 85, 期 2, 页码 97-106出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.biopsych.2018.08.018
关键词
Cytokine-glucocorticoid feedback; Cytokines; Hypothalamic pituitary adrenal; Pregnancy; Stress; Transgenerational
资金
- National Institute of Mental Health [K23MH107831, K23MH102360, P50 MH099910]
- National Institute of Allergy and Infectious Diseases [AI124084]
- Office of Research on Women's Health [P50 MH099919, K12HD085848]
- Brain and Behavior Research Foundation NARSAD Young Investigator Award
During pregnancy, programming of the fetal central nervous system establishes vulnerabilities for emergence of neuropsychiatric phenotypes later in life. Psychosocial influences during pregnancy, such as stressful life events and chronic stress, correlate with offspring neuropsychiatric disorders and inflammation, respectively. Stress promotes inflammation, but the role of inflammation as a mediator between maternal psychosocial stress and offspring neuropsychiatric outcomes has not been extensively studied in humans. This review summarizes clinical evidence linking specific types of stress to maternal inflammatory load during pregnancy. We propose that inflammation is a mediator in the relationship between psychosocial stress and offspring neuropsychiatric outcomes, potentially influenced by poor maternal glucocorticoid-immune coordination. We present relevant experimental animal research supporting this hypothesis. We conclude that clinical and preclinical research supports the premise that stress-induced maternal immune activation contributes in part to prenatal programming of risk. Programming of risk is likely due to a combination of vulnerabilities, including multiple or repeated inflammatory events; timing of such events; poor maternal regulation of inflammation; genetic vulnerability; and lifestyle contributors.
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