Maternal Immune Activation Induced by Prenatal Lipopolysaccharide Exposure Leads to Long-Lasting Autistic-like Social, Cognitive and Immune Alterations in Male Wistar Rats.

Researchers gave pregnant rats a substance that causes infection-like immune responses, then studied their babies as they grew up. The offspring showed autism-like behaviors including social difficulties, communication problems, thinking challenges, and repetitive behaviors. They also had ongoing inflammation. This animal research helps us understand how infections during pregnancy might increase autism risk.

This animal study examined how maternal immune activation during pregnancy affects offspring development in rats. Pregnant rats were exposed to lipopolysaccharide (LPS) to trigger immune responses, and researchers tracked behavioral and immune changes in offspring from infancy through adulthood. Results showed that maternal immune activation led to persistent deficits in communication, social behavior, and cognition, alongside stereotypic behaviors and altered inflammatory markers. The study provides experimental evidence supporting the hypothesis that maternal infections or inflammation during pregnancy may contribute to increased risk of neurodevelopmental disorders, including autism-like traits, in offspring.

Supports the importance of preventing and treating maternal infections during pregnancy. May inform autism risk counseling for families. Contributes to understanding of immune-brain connections in neurodevelopment, though human studies needed to confirm clinical relevance.

Animal study using rats, so findings may not directly translate to humans. Sample size not reported. Study design details unclear from abstract. Limited information about specific behavioral measures or effect sizes.

Several studies have supported the association between maternal immune activation (MIA) caused by exposure to pathogens or inflammation during critical periods of gestation and an increased susceptibility to the development of various psychiatric and neurological disorders, including autism and other neurodevelopmental disorders (NDDs), in the offspring. In the present work, we aimed to provide extensive characterization of the short- and long-term consequences of MIA in the offspring, both at the behavioral and immunological level. To this end, we exposed Wistar rat dams to Lipopolysaccharide and tested the infant, adolescent and adult offspring across several behavioral domains relevant to human psychopathological traits. Furthermore, we also measured plasmatic inflammatory markers both at adolescence and adulthood.

Our results support the hypothesis of a deleterious impact of MIA on the neurobehavioral development of the offspring: we found deficits in the communicative, social and cognitive domains, together with stereotypic-like behaviors and an altered inflammatory profile at the systemic level. Although the precise mechanisms underlying the role of neuroinflammatory states in neurodevelopment need to be clarified, this study contributes to a better understanding of the impact of MIA on the risk of developing behavioral deficits and psychiatric illness in the offspring.