Presenting Author: Olivia Bunton
, Undergraduate Research Assistant at Univ. of Minnesota, Duluth
Abstract:
Preeclampsia (PreE), a hypertensive disorder in pregnancy, is the global leading cause of maternal-fetal morbidity and mortality. Previously, we noted immune cell changes at gestational day 18 (GD18) in offspring of PreE. While offspring cardiovascular and metabolic risks are increasingly studied, there is comparatively less investigation into the persistence of immune cell changes post-PreE in offspring. Our study aims to assess the persistence of immune cell changes observed in PreE-affected offspring on GD18 (term in mice) postnatally into adulthood. PreE was induced in virgin C57BL/6J female mice by infusion of vasopressin (AVP) or saline via subcutaneous infusion throughout gestation. Offspring were euthanized at postnatal week 1, 7, or 12 for experimental outcomes. Offspring body and heart weight were recorded, and total urine protein was quantified. Flow cytometry was used to evaluate immune cell populations. Total T cells, as well as CD4+ and CD8+ T cells, were increased in the offspring of PreE postnatally. Surprisingly, there was also an increase in total B cells and isotype-switched B cells, while macrophage populations were decreased in offspring from AVP-induced dams. Our results confirm that immune cell alterations triggered by PreE persist in offspring postnatally. Ongoing research focuses on unraveling the implications of these immune cell changes in potentially shaping responses to pathogens and the development of autoimmune diseases later in life.
Persistent immune shifts: Unveiling the legacy of vasopressin-triggered preeclampsia in offspring
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Poster
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Date: May 4 Presentation Time: 11:30 AM to 12:45 PM Room: Exhibit Hall F1