Rachel L Maguire1,2, John S House1,3,4, Dillon T Lloyd1, Harlyn G Skinner1,3, Terrence K Allen5, Asifa Mohamed Raffi1, David A Skaar1,3, Sarah S Park1, Lauren E McCullough6, Scott H Kollins7, Staci D Bilbo8, David N Collier3,9,10, Susan K Murphy2, Bernard F Fuemmeler11, Kymberly M Gowdy12, Cathrine Hoyo1,3. 1. Department of Biological Sciences, North Carolina State University, Raleigh, North Carolina, USA. 2. Department of Obstetrics and Gynecology, Duke University, Durham, North Carolina, USA. 3. Center for Human Health and the Environment, North Carolina State University, Raleigh, North Carolina, USA. 4. Division of Intramural Research, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA. 5. Department of Anesthesiology, Duke University, Durham, North Carolina, USA. 6. Department of Epidemiology, Emory University, Atlanta, Georgia, USA. 7. Department of Psychiatry and Behavioral Sciences, Duke University, Durham, North Carolina, USA. 8. Department of Psychology and Neuroscience, Duke University, Durham, North Carolina, USA. 9. Department of Pediatrics, Brody School of Medicine, East Carolina University, Greenville, North Carolina, USA. 10. East Carolina Diabetes and Obesity Institute, East Carolina University, Greenville, North Carolina, USA. 11. Department of Health Behavior and Policy, Virginia Commonwealth University, Richmond, Virginia, USA. 12. Pulmonary, Critical Care and Sleep Medicine, The Ohio State University Wexner Medical Center, Davis Heart and Lung Research Institute, Columbus, Ohio, USA.
Abstract
BACKGROUND: Although maternal systemic inflammation is hypothesized to link maternal pre-pregnancy obesity to offspring metabolic dysfunction, patient empirical data are limited. OBJECTIVES: In this study, we hypothesized that pre-pregnancy obesity alters systemic chemo/cytokines concentrations in pregnancy, and this alteration contributes to obesity in children. METHODS: In a multi-ethnic cohort of 361 mother-child pairs, we measured prenatal concentrations of plasma TNF-α, IL-6, IL-8, IL-1β, IL-4, IFN-γ, IL-12 p70 subunit, and IL-17A using a multiplex ELISA and examined associations of pre-pregnancy obesity on maternal chemo/cytokine levels, and associations of these cytokine levels with offspring body mass index z score (BMI-z) at age 2-6 years using linear regression. RESULTS: After adjusting for maternal smoking, ethnicity, age, and education, pre-pregnancy obesity was associated with increased concentrations of TNF-α (P = .026) and IFN-γ (P = .06). While we found no evidence for associations between TNF-α concentrations and offspring BMI-z, increased IFN-γ concentrations were associated with decreased BMI-z (P = .0002), primarily in Whites (P = .0011). In addition, increased maternal IL-17A concentrations were associated with increased BMI-z in offspring (P = .0005) with stronger associations in African Americans (P = .0042) than Whites (P = .24). CONCLUSIONS: Data from this study are consistent with maternal obesity-related inflammation during pregnancy, increasing the risk of childhood obesity in an ethnic-specific manner.
BACKGROUND: Although maternal systemic inflammation is hypothesized to link maternal pre-pregnancy obesity to offspring metabolic dysfunction, patient empirical data are limited. OBJECTIVES: In this study, we hypothesized that pre-pregnancy obesity alters systemic chemo/cytokines concentrations in pregnancy, and this alteration contributes to obesity in children. METHODS: In a multi-ethnic cohort of 361 mother-child pairs, we measured prenatal concentrations of plasma TNF-α, IL-6, IL-8, IL-1β, IL-4, IFN-γ, IL-12 p70 subunit, and IL-17A using a multiplex ELISA and examined associations of pre-pregnancy obesity on maternal chemo/cytokine levels, and associations of these cytokine levels with offspring body mass index z score (BMI-z) at age 2-6 years using linear regression. RESULTS: After adjusting for maternal smoking, ethnicity, age, and education, pre-pregnancy obesity was associated with increased concentrations of TNF-α (P = .026) and IFN-γ (P = .06). While we found no evidence for associations between TNF-α concentrations and offspring BMI-z, increased IFN-γ concentrations were associated with decreased BMI-z (P = .0002), primarily in Whites (P = .0011). In addition, increased maternal IL-17A concentrations were associated with increased BMI-z in offspring (P = .0005) with stronger associations in African Americans (P = .0042) than Whites (P = .24). CONCLUSIONS: Data from this study are consistent with maternal obesity-related inflammation during pregnancy, increasing the risk of childhood obesity in an ethnic-specific manner.
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