Maternal immune activation induces autism-like behavior and reduces brain-derived neurotrophic factor levels in the hippocampus and offspring cortex of C57BL/6 mice.

This animal study looked at how infections during pregnancy might affect children's development. Researchers triggered immune responses in pregnant mice and studied their offspring. Adult offspring showed autism-like behaviors including less social interaction and repetitive movements. They also had lower levels of important brain proteins.

However, younger offspring appeared normal, suggesting these effects develop over time. This research helps us understand how maternal illness during pregnancy might contribute to autism risk.

This preclinical study investigated autism-like behaviors in mice whose mothers experienced immune activation during pregnancy. Researchers used lipopolysaccharide (LPS) to trigger maternal immune activation (MIA) and examined offspring at 28 and 60 days of age. Adult mice (60 days) showed reduced social interaction and increased repetitive self-grooming behaviors characteristic of autism spectrum disorder. Neurochemical analysis revealed decreased brain-derived neurotrophic factor (BDNF) levels in the hippocampus at both time points, with interleukin-17A (IL-17A) levels reduced only at 60 days.

Notably, younger mice (28 days) did not exhibit these behavioral changes, suggesting developmental timing is crucial. The findings support the hypothesis that maternal immune activation during pregnancy may contribute to autism-like behaviors through disrupted neurotrophic factor signaling.

Findings suggest maternal immune activation during pregnancy may increase autism risk through disrupted brain development. Early neurochemical changes precede behavioral symptoms, indicating potential windows for intervention. Results support monitoring maternal health during pregnancy and investigating neuroprotective strategies targeting BDNF signaling pathways.

This is an animal model study using mice, so findings may not directly translate to humans. Sample size not reported, limiting statistical power assessment. Study focused on specific brain regions and time points, potentially missing other relevant changes. LPS-induced immune activation may not perfectly replicate human maternal infections during pregnancy.

Prenatal factors such as viral or bacterial infections occurring mainly during the first trimesters of pregnancy can increase the incidence of autism spectrum disorder (ASD) in children. In an animal model, it is already known that maternal immune activation (MIA) induces autistic-like behavior. However, it is unclear whether this behavior presents itself in young animals. In this preclinical experimental study, we investigated in the offspring of C57BL/6 female mice submitted to MIA with lipopolysaccharide (LPS), typically altered behaviors in ASD, such as social interaction and stereotyped self-grooming movement, as well as the levels of the brain-derived neurotrophic factor (BDNF) and interleukin 17A (IL-17A) in the hippocampus and cortex, at 28 and 60 days.

Adult animals aged 60 days, offspring of females submitted to MIA, showed a decrease in the time of social interaction and an increase in the number of self-cleaning movements. In the hippocampus of the offspring of females submitted to MIA, a decrease in BDNF levels was found at 28 days and 60 days of life, and a decrease in IL-17A levels only at 60 days. The levels of BDNF and IL-17A did not change in the cortex of the offspring of mice submitted to MIA at the evaluated times. Young animals aged 28 days still showed typical behavior, without social deficits and stereotyped movements that characterize ASD, which suggests that at this age it is still not possible to observe the repercussions of MIA in this model.

In the neurochemical issues of the hippocampal region, impairment of BDNF levels has already been demonstrated, which may be an important factor for the observation of ASD-like behaviors in adult mice at 60 days.