Increasing maternal body mass index during pregnancy increases neonatal intensive care unit admission in near and full-term infants

Suk, Debbie; Kwak, Taehee; Khawar, Nayaab; VanHorn, Samantha; Salafia, Carolyn M.; Gudavalli, Madhu; Narula, Pramod

doi:10.3109/14767058.2015.1124082

Cited by 20 publications

(36 citation statements)

References 27 publications

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“…In line with the developmental origins of health and disease hypothesis, epidemiologic studies have linked pregravid obesity with detrimental cardiometabolic, neurocognitive, and behavioral outcomes in the offspring . More recent studies have also revealed a significant impact on the fetal immune system indicated by a higher incidence of bacterial and viral infections in neonates born to mothers with obesity that require admission to the neonatal intensive care unit . Moreover, the higher incidence of pregravid obesity has been implicated in the rising prevalence of allergic diseases (childhood wheeze and atopy) and asthma during early life, childhood, and adolescence .…”

Section: Introductionmentioning

confidence: 96%

Impact of pregravid obesity on maternal and fetal immunity: Fertile grounds for reprogramming

Sureshchandra

Marshall

Messaoudi

2019

Journal of Leukocyte Biology

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Maternal pregravid obesity results in several adverse health outcomes during pregnancy, including increased risk of gestational diabetes, preeclampsia, placental abruption, and complications at delivery. Additionally, pregravid obesity and in utero exposure to high fat diet have been shown to have detrimental effects on fetal programming, predisposing the offspring to adverse cardiometabolic, endocrine, and neurodevelopmental outcomes. More recently, a deeper appreciation for the modulation of offspring immunity and infectious disease‐related outcomes by maternal pregravid obesity has emerged. This review will describe currently available animal models for studying the impact of maternal pregravid obesity on fetal immunity and review the data from clinical and animal model studies. We also examine the burden of pregravid obesity on the maternal–fetal interface and the link between placental and systemic inflammation. Finally, we discuss future studies needed to identify key mechanistic underpinnings that link maternal inflammatory changes and fetal cellular reprogramming events.

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Section: Introductionmentioning

confidence: 96%

Impact of pregravid obesity on maternal and fetal immunity: Fertile grounds for reprogramming

Sureshchandra

Marshall

Messaoudi

2019

Journal of Leukocyte Biology

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“…Apart from the impact of maternal obesity on increasing numerous fetal and perinatal health risks, 4-7 studies also demonstrate continued long-term risks for offspring including childhood obesity, 8, 9 metabolic dysregulation, 9 asthma 2, 10 and increased inflammation. 10-12 Additionally, as defined by the 2009 Institute of Medicine (IOM) guidelines, 13 low as well as excessive gestational weight gain (EGWG) are associated with increased infant mortality, 14, 15 large for gestational age, and neonatal intensive care admissions.…”

Section: Introductionmentioning

confidence: 99%

Impact of parental obesity on neonatal markers of inflammation and immune response

et al. 2016

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Background/Objectives Maternal obesity may influence neonatal and childhood morbidities through increased inflammation and/or altered immune response. Less is known about paternal obesity. We hypothesized that excessive parental weight contributes to elevated inflammation and altered immunoglobulin (Ig) profiles in neonates. Subjects/Methods In the Upstate KIDS Study maternal pre-pregnancy body mass index (BMI) was obtained from vital records and paternal BMI from maternal report. Biomarkers were measured from newborn dried blood spots (DBS) among neonates whose parents provided consent. Inflammatory scores were calculated by assigning one point for each of 5 pro-inflammatory biomarkers above the median and one point for an anti-inflammatory cytokine below the median. Linear regression models and generalized estimating equations were used to estimate mean differences (β) and 95% confidence intervals (CI) in the inflammatory score and Ig levels by parental overweight/obesity status compared to normal weight. Results Among 2974 pregnancies, 51% were complicated by excessive maternal weight (BMI>25), 73% by excessive paternal weight, and 28% by excessive gestational weight gain. Maternal BMI categories of overweight (BMI 25.0-29.9) and obese class II/III (BMI≥35) were associated with increased neonatal inflammation scores (β=0.12, 95% CI: 0.02, 0.21; p=0.02, and β=0.13, CI: −0.002, 0.26; p=0.05, respectively) but no increase was observed in the obese class I group (BMI 30-34.9). Mothers with class I and class II/III obesity had newborns with increased IgM levels (β=0.11, CI: 0.04, 0.17; p=0.001 and β=0.12, CI: 0.05, 0.19); p<0.001, respectively). Paternal groups of overweight, obese class I and obese class II/III had decreased neonatal IgM levels (β=−0.08, CI: −0.13,-0.03, p=0.001; β=−0.07, CI: −0.13, −0.01, p=0.029 and β=−0.11, CI:−0.19,-0.04, p=0.003, respectively). Conclusions Excessive maternal weight was generally associated with increased inflammation and IgM supporting previous observations of maternal obesity and immune dysregulation in offspring. The role of paternal obesity requires further study.

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“…For the fetus, complications include increased risk of stillbirth, abnormal growth, and cardiac or neural tube defects (1,4). Moreover, neonates born to obese mothers are at increased risk of bacterial sepsis and necrotizing enterocolitis, requiring admission to the neonatal intensive care unit (5,6). Some adverse health outcomes for the offspring persist into adulthood, including increased susceptibility to respiratory infections such as respiratory syncytial virus (7,8), asthma (9), wheezing (10), cancer (11), type 2 diabetes (12), and cardiovascular disease (13), culminating in an increased risk for all-cause offspring mortality (14).…”

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confidence: 99%

Maternal Pregravid Obesity Remodels the DNA Methylation Landscape of Cord Blood Monocytes Disrupting Their Inflammatory Program

Sureshchandra

Wilson

Rais

et al. 2017

The Journal of Immunology

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Prepregnancy maternal obesity is associated with adverse outcomes for the offspring, including increased incidence of neonatal bacterial sepsis and necrotizing enterocolitis. We recently reported that umbilical cord blood (UCB) monocytes from babies born to obese mothers generate a reduced IL-6/TNF-α response to TLR 1/2 and 4 ligands compared to those collected from lean mothers. These observations suggest altered development of the offspring's immune system, which in turn results in dysregulated function. We therefore investigated transcriptional and epigenetic differences within UCB monocytes stratified by prepregnancy maternal body mass index. We show that UCB monocytes from babies born to obese mothers generate a dampened response to LPS stimulation compared with those born to lean mothers, at the level of secreted immune mediators and transcription. Because gene expression profiles of resting UCB monocytes from both groups were comparable, we next investigated the role of epigenetic differences. Indeed, we detected stark differences in methylation levels within promoters and regulatory regions of genes involved in TLR signaling in resting UCB monocytes. Interestingly, the DNA methylation status of resting cells was highly predictive of transcriptional changes post-LPS stimulation, suggesting that cytosine methylation is one of the dominant mechanisms driving functional inadequacy in UCB monocytes obtained from babies born to obese mothers. These data highlight a potentially critical role of maternal pregravid obesity-associated epigenetic changes in influencing the function of an offspring's monocytes at birth. These findings further our understanding of mechanisms that explain the increased risk of infection in neonates born to mothers with high prepregnancy body mass index.

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Increasing maternal body mass index during pregnancy increases neonatal intensive care unit admission in near and full-term infants

Cited by 20 publications

References 27 publications

Impact of pregravid obesity on maternal and fetal immunity: Fertile grounds for reprogramming

Impact of pregravid obesity on maternal and fetal immunity: Fertile grounds for reprogramming

Impact of parental obesity on neonatal markers of inflammation and immune response

Maternal Pregravid Obesity Remodels the DNA Methylation Landscape of Cord Blood Monocytes Disrupting Their Inflammatory Program

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