@article {5892, title = {Inflammation: A Proposed Intermediary Between Maternal Stress and Offspring Neuropsychiatric Risk}, journal = {Biol Psychiatry}, volume = {85}, number = {2}, year = {2019}, note = {1873-2402
Hantsoo, Liisa
Kornfield, Sara
Anguera, Montserrat C
Epperson, C Neill
K23 MH107831/MH/NIMH NIH HHS/United States
K12 HD085848/HD/NICHD NIH HHS/United States
R21 AI124084/AI/NIAID NIH HHS/United States
K23 MH102360/MH/NIMH NIH HHS/United States
P50 MH099910/MH/NIMH NIH HHS/United States
Journal Article
Review
United States
Biol Psychiatry. 2019 Jan 15;85(2):97-106. doi: 10.1016/j.biopsych.2018.08.018. Epub 2018 Sep 5.}, month = {Jan 15}, pages = {97-106}, edition = {2018/10/14}, abstract = {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.}, keywords = {Cytokine-glucocorticoid feedback, Cytokines, Hypothalamic pituitary adrenal, Pregnancy, stress, Transgenerational}, isbn = {0006-3223}, doi = {10.1016/j.biopsych.2018.08.018}, author = {Hantsoo, L. and Kornfield, S. and Anguera, M. C. and Epperson, C. N.} }