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Chronic arsenic exposure affects over 140 million people globally. While arsenic easily crosses the placenta, the specific mechanisms impacting placental immune cell populations and fetal health are unclear. Maternal arsenic exposure is epidemiologically linked to increased infection risk, mortality, and cancer susceptibility in offspring, emphasizing the importance of understanding placentally-mediated immune effects.

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Background/objectives: Respiratory syncytial virus (RSV) is the leading cause of severe respiratory disease in infants worldwide. Maternal immunization to protect younger infants is supported by evidence that virus-neutralizing antibodies, which are efficiently transferred across the placenta from mother to fetus, are a primary immune mediator of protection. In maternal RSV vaccine studies, estimates of correlates of protection are elusive because many factors of maternal-fetal immunobiology and disease characteristics must be considered for the estimates.

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Microplastics (MPs) are emerging environmental pollutants. Pregnancy and infancy are sensitive windows for environmental exposure. However, few studies have investigated the presence of MPs in mother-infant pairs, or the exposure source.

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The placenta plays a critical role in nutrient and oxygen exchange during pregnancy, yet the effects of medicinal drugs on this selective barrier remain poorly understood. To overcome this, this study presents a cost-effective bioimpedance spectroscopy (BIS) system to assess tight junction integrity and monolayer formation in BeWo b30 cells, a widely used model of the multinucleated maternal-fetal exchange surface of the placental barrier. Cells were cultured on collagen-coated porous membranes and treated with forskolin to induce controlled syncytialization.

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A low pre-existing anti-NS1 humoral immunity to DENV is associated with microcephaly development after gestational ZIKV exposure.

PLoS Negl Trop Dis

January 2025

División de Inmunología, Programa de Medicina, Facultad de Ciencias de la Salud, Universidad Surcolombiana, Neiva, Huila, Colombia.

Background: Gestational Zika virus (ZIKV) infection is associated with the development of congenital Zika syndrome (CZS), which includes microcephaly and fetal demise. The magnitude and quality of orthoflavivirus-specific humoral immunity have been previously linked to the development of CZS. However, the role of ZIKV NS1-specific humoral immunity in mothers and children with prenatal ZIKV exposure and CZS remains undefined.

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