Maternal infection perturbs fetal brain development through IL-6 signaling
Sunday, Nov 10, 2013, 3:00 PM - 4:00 PM
++C.07.a. Autism: Genetic and animal models
, W.-L. WU, E. Y. HSIAO, P. H. PATTERSON;
Div. of Biol., Caltech, Pasadena, CA
Epidemiologic studies identify maternal infection as a risk factor for autism and schizophrenia in the offspring. To understand the mechanism of how maternal infection alters fetal brain development, we use a mouse model in which injection of the viral mimic poly(I:C) at mid-gestation elicits maternal immune activation (MIA). MIA offspring exhibit autistic- and schizophrenia-like behaviors as well as neuropathology characteristic of each of these disorders. Prior work demonstrated that maternal interleukin-6 (IL-6) is a key cytokine that mediates the effects of MIA on the fetus. The receptor for IL-6, IL-6Rα, is expressed in brain regions associated with pathology in autism and schizophrenia. To examine where this cytokine acts, we are studying patterns of activation of IL-6 signaling in the fetal brain. First, we demonstrate that IL-6 mRNA and protein increase in fetal brain 3 hours following maternal poly(I:C) injection. Second, we find that highly selective regions of the embryonic brain respond to MIA: phospho-STAT3 (pSTAT3) immunostaining is elevated in the hindbrain and cerebellar primordium, and laser capture micro-dissection analysis of the JAK/STAT signaling pathway yields results consistent with the immunostaining. To further examine the role of IL-6, we have generated tissue-specific IL-6Rα knockout mice.
MATERNAL IMMUNE ACTIVATION
Caltech Undergraduate Research Fellowship (SURF)
Amgen Scholars Program at Caltech
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