Uncontrolled inflammation during pregnancy, coined ‘maternal immune activation’ (MIA), may induce behavioral phenotypes and brain pathologies relevant to autism in affected offspring. In recent work, supported in part by a previous SFARI Research Award, Jun Huh’s laboratory used a mouse MIA model to demonstrate that gut-residing bacteria that induce TH17 cell biogenesis in pregnant mothers may make offspring more susceptible to developing neurodevelopmental abnormalities1.
In the current proposal, Huh aims to identify human-derived bacteria that can colonize the maternal gut and prevent maternal TH17 cell-dependent induction of neurodevelopmental abnormalities in offspring. To do so, the group will perform tests with human commensal bacteria that are known to promote anti-inflammatory responses.
Identifying bacteria that suppress MIA phenotypes in mice may provide a novel avenue to reduce dysregulated inflammation in pregnant women and the subsequent risk of inflammation-induced neurodevelopment disorders in their children.