Maternal infection during pregnancy is a known risk factor for offspring mental health disorders. Animal models of maternal immune activation (MIA) have implicated specific cellular and molecular etiologies of psychiatric illness, but most rely on pathogen mimetics. Here, we developed a mouse model of live H3N2 influenza A virus (IAV) infection during pregnancy that induces a robust inflammatory response but is sublethal to both dams and offspring. We observed lung inflammatory cytokine production and severely diminished weight gain in IAV-infected dams. This was accompanied by immune cell infiltration in the placenta and partial breakdown of placental integrity. However, indications of IL-17A signaling and fetal neuroinflammation, which are hallmarks of mimetic-induced MIA, were not detected. Our results suggest that mild or moderately pathogenic IAV infection during pregnancy does not inflame the developing fetal brain, and highlight the importance of live pathogen infection models for the study of MIA.

中文翻译：

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中度致病的孕妇甲型流感病毒感染会破坏胎盘的完整性，但会使胎儿的大脑免受伤害

怀孕期间的母体感染是已知的后代心理健康障碍的危险因素。孕产妇免疫激活（MIA）的动物模型涉及精神病的特定细胞和分子病因，但大多数依赖病原体模拟物。在这里，我们开发了一种在怀孕期间感染H3N2甲型流感活病毒（IAV）的小鼠模型，该模型可诱导强烈的炎症反应，但对大坝和后代均具有致命性。我们观察到在IAV感染的大坝中肺炎性细胞因子的产生和体重增加的严重减少。这伴随着免疫细胞在胎盘中的浸润和胎盘完整性的部分破坏。但是，没有检测到IL-17A信号和胎儿神经炎症的迹象，这是模拟物诱导的MIA的标志。