Inflammation: A Proposed Intermediary Between Maternal Stress and Offspring Neuropsychiatric Risk

TitleInflammation: A Proposed Intermediary Between Maternal Stress and Offspring Neuropsychiatric Risk
Publication TypeJournal Article
AuthorsHantsoo, L., S. Kornfield, M. C. Anguera, and C. N. Epperson
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.
Title Inflammation: A Proposed Intermediary Between Maternal Stress and Offspring Neuropsychiatric Risk
Publication Title Biol Psychiatry
Publication Type Journal Article
Published Year 2019
Authors L. Hantsoo; S. Kornfield; M.C. Anguera; C.N. Epperson
Edition 2018/10/14
Accession Number 30314641
Number 2
ISBN Number 0006-3223
Grant List
-

JOIN THE CONVERSATION

For breaking news and to stay connected, follow us on social media. Sign up to get our E-News delivered straight to your inbox.