Maternal gut bacteria promote neurodevelopmental abnormalities in mouse offspring.

ABSTRACT: Maternal immune activation (MIA) contributes to behavioural abnormalities associated with neurodevelopmental disorders in both primate and rodent offspring. In humans, epidemiological studies suggest that exposure of fetuses to maternal inflammation increases the likelihood of developing autism spectrum disorder. In pregnant mice, interleukin-17a (IL-17a) produced by T helper 17 (T_H17) cells (CD4⁺ T helper effector cells involved in multiple inflammatory conditions) induces behavioural and cortical abnormalities in the offspring exposed to MIA. However, it is unclear whether other maternal factors are required to promote MIA-associated phenotypes. Moreover, the underlying mechanisms by which MIA leads to T cell activation with increased IL-17a in the maternal circulat

SUBMITTER: Kim S 

PROVIDER: S-EPMC5870873 | biostudies-literature | 2017 Sep

REPOSITORIES: biostudies-literature