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

<p dir="ltr">Data for the manuscript<b>:</b></p><p dir="ltr"><b>'Adverse maternal and fetal outcomes in mouse models of prenatal infections'</b></p><p dir="ltr">Evgeniya V Shmeleva, Delia Hawkes, Cecilia Lusuardi, Yasmin Adewusi, Salvatore Valenti, Francesco Colucci*</p><p dir="ltr"><b>Abstract</b></p><p dir="ltr">Prenatal 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: <i>Toxoplasma gondii</i> (intraperitoneal), vaccinia virus (intranasal), murine cytomegalovirus (intravenous) and influenza A virus (intranasal). We found markedly different effects on maternal morbidity and mortality, with <i>T. gondii</i> 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 <i>T.gondii </i>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 <i>T. gondii</i> 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.</p>