Fetal hemodynamic changes in pregnant women with influenza <scp>AH1N1</scp> infection and reduced arterial partial pressure of oxygen

Hernández‐Andrade, Edgar; Damián, Ricardo Figueroa; Cérbulo-Vázquez, Arturo; Benavides‐Serralde, J. A.; Borbon, G. P.; Ramírez, Javier

doi:10.1002/uog.13417

Cited by 3 publications

(1 citation statement)

References 4 publications

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“…Preclinical studies have also demonstrated significantly altered placental vascularization, vascular remodeling, and oxygen transport in response to maternal infection (Tabata et al, 2012; Conroy et al, 2013; Hirsch et al, 2018; McDonald et al, 2018; Phillips et al, 2018). In humans, maternal infections including influenza, Helicobacter pylori , malaria, and HIV have been associated with impaired maternal and fetal hemodynamics (e.g., high arterial resistance) (Dorman et al, 2002; Griffin et al, 2012; Hernandez-Andrade et al, 2014; McClure et al, 2014; Di Simone et al, 2017; Ome-Kaius et al, 2017). The available evidence implicates abnormalities in placental vascularization and function as a common driver behind infection-induced adverse birth outcomes, even in non-congenital infections.…”

Section: Maternal Infection Disrupts Placental Vascular Developmentmentioning

confidence: 99%

The Impact of Infection in Pregnancy on Placental Vascular Development and Adverse Birth Outcomes

et al. 2019

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Healthy fetal development is dependent on nutrient and oxygen transfer via the placenta. Optimal growth and function of placental vasculature is therefore essential to support in utero development. Vasculogenesis, the de novo formation of blood vessels, and angiogenesis, the branching and remodeling of existing vasculature, mediate the development and maturation of placental villi, which form the materno-fetal interface. Several lines of evidence indicate that systemic maternal infection and consequent inflammation can disrupt placental vasculogenesis and angiogenesis. The resulting alterations in placental hemodynamics impact fetal growth and contribute to poor birth outcomes including preterm delivery, small-for-gestational age (SGA), stillbirth, and low birth weight (LBW). Furthermore, pathways involved in maternal immune activation and placental vascularization parallel those involved in normal fetal development, notably neurovascular development. Therefore, immune-mediated disruption of angiogenic pathways at the materno-fetal interface may also have long-term neurological consequences for offspring. Here, we review current literature evaluating the influence of maternal infection and immune activation at the materno-fetal interface and the subsequent impact on placental vascular function and birth outcome. Immunomodulatory pathways, including chemokines and cytokines released in response to maternal infection, interact closely with the principal pathways regulating placental vascular development, including the angiopoietin-Tie-2, vascular endothelial growth factor (VEGF), and placental growth factor (PlGF) pathways. A detailed mechanistic understanding of how maternal infections impact placental and fetal development is critical to the design of effective interventions to promote placental growth and function and thereby reduce adverse birth outcomes.

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Section: Maternal Infection Disrupts Placental Vascular Developmentmentioning

confidence: 99%

The Impact of Infection in Pregnancy on Placental Vascular Development and Adverse Birth Outcomes

et al. 2019

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Severe maternal infectious morbidity during the second half of pregnancy is an independent risk factor for a small for gestational age neonate

Kedar¹,

Erez²,

Novak³

et al. 2022

European Journal of Obstetrics & Gynecology and Reproductiv

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Pregnant Women Infected with Pandemic H1N1pdm2009 Influenza Virus Displayed Overproduction of Peripheral Blood CD69+ Lymphocytes and Increased Levels of Serum Cytokines

et al. 2014

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The first pandemic of the 21st century occurred in 2009 and was caused by the H1N1pdm influenza A virus. Severe cases of H1N1pdm infection in adults are characterized by sustained immune activation, whereas pregnant women are prone to more severe forms of influenza, with increased morbi-mortality. During the H1N1pdm09 pandemic, few studies assessed the immune status of infected pregnant women. The objective of this study was to evaluate the behavior of several immune markers in 13 H1N1pdm2009 virus-infected pregnant (PH1N1) women, in comparison to pregnant women with an influenza-like illness (ILI), healthy pregnant women (HP) and healthy non-pregnant women (HW). The blood leukocyte phenotypes and the serological cytokine and chemokine concentrations of the blood leukocytes, as measured by flow cytometry, showed that the CD69+ cell counts in the T and B-lymphocytes were significantly higher in the PH1N1 group. We found that pro-inflammatory (TNF-α, IL-1β, IL-6) and anti-inflammatory (IL-10) cytokines and some chemokines (CXCL8, CXCL10), which are typically at lower levels during pregnancy, were substantially increased in the women in the ILI group. Our findings suggest that CD69 overexpression in blood lymphocytes and elevated levels of serum cytokines might be potential markers for the discrimination of H1N1 disease from other influenza-like illnesses in pregnant women.

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Fetal hemodynamic changes in pregnant women with influenza AH1N1 infection and reduced arterial partial pressure of oxygen

Cited by 3 publications

References 4 publications

The Impact of Infection in Pregnancy on Placental Vascular Development and Adverse Birth Outcomes

The Impact of Infection in Pregnancy on Placental Vascular Development and Adverse Birth Outcomes

Severe maternal infectious morbidity during the second half of pregnancy is an independent risk factor for a small for gestational age neonate

Pregnant Women Infected with Pandemic H1N1pdm2009 Influenza Virus Displayed Overproduction of Peripheral Blood CD69+ Lymphocytes and Increased Levels of Serum Cytokines

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