Maternal and early postnatal immune activation produce sex-specific effects on autism-like behaviors and neuroimmune function in mice.
Level 5 - mechanism / opinion, no new human data
Preclinical animal research with no human clinical data.
PubMed 31729416 · doi:10.1038/s41598-019-53294-z
What was done
Timed-pregnant C57BL/6J mice received polyinosinic:polycytidylic acid (Poly I:C) at gestational day 12.5 to produce maternal immune activation (MIA). A subset of offspring received lipopolysaccharide (LPS) on postnatal day 9 for postnatal immune activation (PIA), establishing prenatal, postnatal, and combined two-hit immune activation regimens. Offspring were assessed for autism spectrum disorder-like phenotypes (social interaction, repetitive behavior, ultrasonic vocalizations) and brain expression of pro-inflammatory and anti-inflammatory mRNA and protein.
What was found
The abstract provides no numerical data, effect sizes, or statistical metrics. Early immune activation produced disruptions in social behavior and increases in repetitive behavior that were larger in males than in females. Ultrasonic vocalizations were altered in both sexes. Both sexes showed increases in pro-inflammatory mRNA and protein, whereas expression of anti-inflammatory factors decreased in males but increased in females.
Why it matters
The study outlines a potential neuroimmune mechanism for male-biased vulnerability and female resilience following early-life immune challenge in a model of autism spectrum disorder.
Limits
Findings are based entirely on an animal model and cannot directly establish human etiology. The abstract omits sample sizes, quantitative measurements, effect sizes, p-values, and the specific molecular names of the assayed inflammatory markers.
Cited by
- supports Autism-like phenotypes are modeled in mice by inducing maternal immune activation through bacterial or immune challenge during pregnancy.