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.
To read this article in full you will need to make a payment
Purchase one-time access:
Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online accessOne-time access price info
- For academic or personal research use, select 'Academic and Personal'
- For corporate R&D use, select 'Corporate R&D Professionals'
Subscribe:
Subscribe to Journal of the Neurological SciencesAlready a print subscriber? Claim online access
Already an online subscriber? Sign in
Register: Create an account
Institutional Access: Sign in to ScienceDirect
