Data from: Offspring behavioral outcomes following maternal allergic asthma in the IL-4-deficient mouse

Background: Maternal allergies and asthma during pregnancy have been
associated with increased risk of ASD and ADHD to the child. Previous
rodent studies have demonstrated that inducing a T helper-2 (Th2)-mediated
allergic response during pregnancy leads to an offspring behavioral
phenotype characterized by decreased social interaction and increased
stereotypies. Interleukin-4 is a key signal in the Th2 immune cascade, but
its role in fetal brain development and subsequent impacts of maternal
allergic asthma (MAA) on offspring behavioral deficits have yet to be
determined. Objective: In this study, we investigated whether the absence
of IL-4 signaling would mitigate MAA-induced behavioral changes. Methods:
C57BL/6J and Interleukin-4 knockout (IL-4 KO) mice were sensitized to
ovalbumin and exposed to repeated allergic asthma aerosol inductions
throughout pregnancy. Offspring were assessed on Juvenile Reciprocal
Social Interaction, Elevated Plus Maze, Open Field Exploration, Novel
Object Recognition, Forced Swim, Marble-burying, and Grooming tasks.
Results: MAA during pregnancy resulted in decreased social interactions in
male C57 offspring and impaired memory performance in both male and female
C57 mice. These deficits were not observed in IL-4 KO mice exposed to MAA.
However, we observed genotype effects in IL-4 KO mice including altered
motor performance and anxiety-associated responses. Conclusion:
MAA-induced social and cognitive behavioral alterations are IL-4
dependent. IL-4KO offspring display genotype-specific differences
suggesting IL-4 signaling is important for typical developmental
processes.