Abstract Body

In humans, epidemiological studies suggest that fetuses' exposure to maternal inflammation increases the likelihood of developing Autism Spectrum Disorder (ASD). We previously demonstrated that interleukin-17a (IL-17a) produced by Th17 cells (CD4+ T helper effector cells involved in multiple autoimmune and inflammatory diseases) is required in pregnant mice to induce behavioral abnormalities in offspring exposed to maternal immune activation (MIA). Furthermore, we and others showed that MIA-induced phenotypes in offspring require maternal intestinal bacteria that promote Th17 cell differentiation. Pregnant mice colonized with a mouse or human commensal bacteria inducing intestinal Th17 cells were more likely to produce offspring with MIA-associated behavioral abnormalities.

These and our more recent data suggest that the immune system and its modulation by the gut microbiota might impact the developing brain and potentially the adult brain to shape animal behavior. I will discuss our ongoing efforts to decipher gut bacteria's modulatory roles in affecting brain function.