Prenatal stress causes intrauterine inflammation and serotonergic dysfunction, and long-term behavioral deficits through microbe- and CCL2-dependent mechanisms.

ABSTRACT: Prenatal stress (PNS) is associated with neuropsychiatric disorders in offspring, including anxiety, depression, and autism spectrum disorders. There is mounting evidence that these behavioral phenotypes have origins in utero. Maternal microbes, inflammation, and serotonergic dysfunction have been implicated as potential mediators of the behavioral consequences of PNS; whether and how these systems interact is unclear. Here, we examine the effects of PNS in utero using late-gestation maternal restraint stress in wild-type (WT), germ-free (GF), and CCL2^-/- genetic knock-out (KO) mice. In WT mice, PNS leads to placental and fetal brain inflammation, including an elevation in the chemokine CCL2. This inflammation is largely absent in GF mice, indicating the cr

SUBMITTER: Chen HJ 

PROVIDER: S-EPMC7297973 | biostudies-literature | 2020 Jun

REPOSITORIES: biostudies-literature