Abstract
Poor immune function increases children’s risk of infection and mortality. Several maternal factors during pregnancy may affect infant immune function during the postnatal period.
We conducted observational analyses within the WASH Benefits Bangladesh randomized controlled trial. We measured biomarkers in 575 pregnant women and postnatally in their children. Maternal biomarkers measured during the first and second trimester of pregnancy included: nutrition status via vitamin D (25-hydroxy-D [25(OH)D]), ferritin, soluble transferrin receptor (sTfR), and retinol binding protein (RBP); cortisol; estriol. Immune markers were assessed in pregnant women at enrollment and their children at ages 14 and 28 months, including: C-reactive protein (CRP), alpha-1-acid glycoprotein (AGP), and thirteen cytokines (including IFN-γ). We generated a standardized sum score of log-transformed cytokines. We analyzed IFN-γ individually because it is a critical immunoregulatory cytokine. All outcomes were pre-specified. We used generalized additive models and reported the mean difference and 95% confidence intervals at the 25th and 75th percentiles of exposure distribution.
At child age 14 months, concentrations of maternal RBP were inversely associated with the cytokine sum score in children (-0.34 adjusted difference between the 25th and 75th percentile [95% confidence interval -0.61, -0.07]), and maternal vitamin A deficiency was positively associated with the cytokine sum score in children (1.02 [0.13, 1.91]). At child age 28 months, maternal RBP was positively associated with IFN-γ in children (0.07 [0.01, 0.14]) while maternal vitamin A deficiency was negatively associated with child AGP (-0.07 [-0.13, -0.02]). Maternal iron deficiency was associated with higher AGP levels in children at age 14 months (0.13 [0.04, 0.23]), and maternal sTfR concentrations were positively associated with child CRP levels at age 28 months (0.18 [0, 0.36]).
Maternal deficiencies in vitamin A or iron during the first two trimesters of pregnancy may shape the trajectory of child immune status.
