Journal
PEDIATRIC ALLERGY AND IMMUNOLOGY
Volume 26, Issue 4, Pages 344-351Publisher
WILEY-BLACKWELL
DOI: 10.1111/pai.12387
Keywords
asthma; cytokine; dendritic cells; maternal obesity; monocytes; T cells; toll-like receptor
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Funding
- NIH [KL2TR000152, R03AI112808]
- National Center for Advancing Translational Sciences of the National Institutes of Health [UL1TR000128]
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BackgroundMaternal obesity is one of the several key factors thought to modulate neonatal immune system development. Data from murine studies demonstrate worse outcomes in models of infection, autoimmunity, and allergic sensitization in offspring of obese dams. In humans, children born to obese mothers are at increased risk for asthma. These findings suggest a dysregulation of immune function in the children of obese mothers; however, the underlying mechanisms remain poorly understood. The aim of this study was to examine the relationship between maternal body weight and the human neonatal immune system. MethodsUmbilical cord blood samples were collected from infants born to lean, overweight, and obese mothers. Frequency and function of major innate and adaptive immune cell populations were quantified using flow cytometry and multiplex analysis of circulating factors. ResultsCompared to babies born to lean mothers, babies of obese mothers had fewer eosinophils and CD4 T helper cells, reduced monocyte and dendritic cell responses to Toll-like receptor ligands, and increased plasma levels of IFN-2 and IL-6 in cord blood. ConclusionThese results support the hypothesis that maternal obesity influences programming of the neonatal immune system, providing a potential link to increased incidence of chronic inflammatory diseases such as asthma and cardiovascular disease in the offspring.
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