Obesity and Maternal-Placental-Fetal Immunology and Health
Meredith Monaco-Brown1, David A Lawrence2,3
1Department of Pediatrics, Bernard and Millie Duker Children's Hospital at Albany Medical Center, Albany, NY, United States.
Insights
Maternal obesity and environmental chemicals disrupt placental immunology, impacting pregnancy outcomes and infant health. This review explores these immune alterations and their links to various neonatal and maternal conditions.
Area of Science:
- Reproductive immunology
- Environmental health
- Perinatal medicine
Background:
- Rising obesity rates in women of childbearing age (29%) are linked to oxidative stress and inflammation.
- Maternal obesity is associated with placental dysfunction, leading to adverse birth outcomes like large for gestational age (LGA) infants and increased neonatal metabolic disease.
- Environmental exposures to endocrine-disrupting and persistent chemicals exacerbate obesity and negatively affect maternal physiology, placental function, and fetal development.
Purpose of the Study:
- To review the scientific literature on how maternal obesity and environmental chemical exposures alter maternal, placental, and fetal immunology.
- To examine the intricate relationship between placental immune function and clinical outcomes, including neonatal conditions and maternal health.
Main Methods:
- Systematic review of existing literature on maternal obesity, environmental chemicals, and placental immunology.
- Analysis of studies investigating placental immune cells (e.g., macrophages, NK cells) and inflammatory mediators (cytokines).
Main Results:
- Maternal obesity and environmental chemicals significantly alter placental immune cell populations and cytokine profiles.
- These immunological changes are associated with adverse pregnancy outcomes such as preeclampsia, preterm birth, and fetal growth restrictions.
- Placental immune dysregulation is linked to a spectrum of neonatal and post-natal conditions, including allergies, metabolic disorders, and neurodevelopmental issues.
Conclusions:
- Maternal obesity and environmental exposures represent critical modulators of placental immunology.
- Understanding these immunomodulatory effects is crucial for improving pregnancy outcomes and addressing long-term infant and maternal health challenges.
- Further research into placental immune function can inform targeted interventions for high-risk pregnancies.
Abstract:
Obesity rates in women of childbearing age is now at 29%, according to recent CDC reports. It is known that obesity is associated with oxidative stress and inflammation, including disruptions in cellular function and cytokine levels. In pregnant women who are obese, associated placental dysfunction can lead to small for gestational age (SGA) infants. More frequently, however, maternal obesity is associated with large for gestational age (LGA) newborns, who also have higher incidence of metabolic disease and asthma due to elevated levels of inflammation. In addition, anthropogenic environmental exposures to "endocrine disrupting" and "forever" chemicals affect obesity, as well as maternal physiology, the placenta, and fetal development. Placental function is intimately associated with the control of inflammation during pregnancy. There is a large amount of literature examining the relationship of placental immunology, both cellular and humoral, with pregnancy and neonatal outcomes. Cells such as placental macrophages and NK cells have been implicated in spontaneous miscarriage, preeclampsia, preterm birth, perinatal neuroinflammation, and other post-natal conditions. Differing levels of placental cytokines and molecular inflammatory mediators also have known associations with preeclampsia and developmental outcomes. In this review, we will specifically examine the literature regarding maternal, placental, and fetal immunology and how it is altered by maternal obesity and environmental chemicals. We will additionally describe the relationship between placental immune function and clinical outcomes, including neonatal conditions, autoimmune disease, allergies, immunodeficiency, metabolic and endocrine conditions, neurodevelopment, and psychiatric disorders.
Related Concept Videos
Obesity
Transcytosis of IgG
IgG molecules from a mother undergo transcytosis starting around 13 weeks of gestation. The amount of IgG transferred and entering the fetal blood circulation increases with...
Development of Immunocompetence
The initial cells that migrate from the fetal thymus settle within the skin and epithelial tissues lining the mouth, digestive tract, and in females, the uterus and vagina. These cells, including skin-based dendritic cells, serve as antigen-presenting cells, playing a key role in T cell activation.
Subsequent T...
Pathophysiology of Diabetes
Type 1 diabetes is characterized by autoimmune-mediated destruction of pancreatic β cells, with environmental factors potentially triggering this process in genetically susceptible individuals. Despite many not having a family history, certain genes increase susceptibility,...
Diabetes Mellitus: Type 2 and Gestational
Psychoneuroimmunology: Diabetes and Cancer


