Data for the manuscript 'Adverse maternal and fetal outcomes in mouse models of prenatal infections'

Data for the manuscript:'Adverse maternal and fetal outcomes in mouse models of prenatal infections'Evgeniya V Shmeleva, Delia Hawkes, Cecilia Lusuardi, Yasmin Adewusi, Salvatore Valenti, Francesco Colucci*AbstractPrenatal infections are a leading cause of adverse pregnancy outcomes, yet the mechanisms underlying pathogen-specific effects on maternal and fetal health remain poorly understood. Here we conducted a comparative analysis of four mouse models of prenatal infection: Toxoplasma gondii (intraperitoneal), vaccinia virus (intranasal), murine cytomegalovirus (intravenous) and influenza A virus (intranasal). We found markedly different effects on maternal morbidity and mortality, with T. gondii causing severe pregnancy-specific pathology leading to complete maternal mortality by 8 days post-infection, despite similar pathogen loads in pregnant and non-pregnant mice. Vaccinia virus caused prenatal morbidity, while cytomegalovirus and influenza induced only mild, transient effects. The maternal mortality in T.gondii infection was most likely due to immunopathology, while vaccinia virus caused prenatal morbidity possibly due to tissue infection. None of the pathogens directly infected the fetuses, yet both T. gondii and vaccinia virus significantly impaired both uterine vascular remodelling and fetal growth. Notably, pregnancy was found to be a modifier of local but not systemic immune responses, with reduced inflammatory cytokine production in uterine tissue of infected pregnant mice compared to non-pregnant controls. These models provide a systematic platform for understanding pathogen-specific mechanisms of pregnancy complications and identifying therapeutic targets.学术论文配套数据集：《产前感染小鼠模型中的母胎不良结局》 作者：埃夫根尼娅·V·施梅列娃（Evgeniya V Shmeleva）、迪莉娅·霍克斯（Delia Hawkes）、塞西莉亚·卢苏阿尔迪（Cecilia Lusuardi）、亚斯明·阿德武西（Yasmin Adewusi）、萨尔瓦托雷·瓦伦蒂（Salvatore Valenti）、弗朗切斯科·科卢奇（Francesco Colucci）* 摘要：产前感染是导致不良妊娠结局的主要诱因之一，但病原体对母胎健康产生的特异性作用机制仍未得到充分阐明。本研究对四种产前感染小鼠模型开展了比较分析，分别为：刚地弓形虫（Toxoplasma gondii，腹腔接种）、痘苗病毒（vaccinia virus，鼻内接种）、小鼠巨细胞病毒（murine cytomegalovirus，静脉接种）以及甲型流感病毒（influenza A virus，鼻内接种）。我们观察到不同模型对母体发病率与死亡率的影响存在显著差异：刚地弓形虫可引发严重的妊娠特异性病理损伤，即便孕鼠与未孕小鼠的病原体载量相近，感染孕鼠仍会在感染后8天内全部死亡。痘苗病毒可引发产前发病，而小鼠巨细胞病毒与甲型流感病毒仅会造成轻微的一过性影响。刚地弓形虫感染所致的母体死亡大概率源于免疫病理损伤，而痘苗病毒引发的产前发病可能与组织感染有关。所有受试病原体均未直接感染胎儿，但刚地弓形虫与痘苗病毒均会显著损害子宫血管重塑与胎儿生长发育。值得注意的是，妊娠可调节局部免疫应答，但不会影响系统性免疫应答：与未孕对照组相比，感染后的孕鼠子宫组织中炎性细胞因子的产生水平有所降低。上述模型为阐明妊娠并发症的病原体特异性作用机制、筛选治疗靶点提供了系统化的研究平台。