Micronutrient status during pregnancy is associated with child immune status in rural Bangladesh.

child immune status iron maternal micronutrients pregnancy vitamin A

Journal

Current developments in nutrition
ISSN: 2475-2991
Titre abrégé: Curr Dev Nutr
Pays: United States
ID NLM: 101717957

Informations de publication

Date de publication:
Aug 2023
Historique:
received: 03 05 2023
revised: 26 06 2023
accepted: 30 06 2023
medline: 10 8 2023
pubmed: 10 8 2023
entrez: 10 8 2023
Statut: epublish

Résumé

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 aimed to evaluate whether maternal micronutrients, stress, estriol, and immune status during the first or second trimester of pregnancy were associated with child immune status in the first two years after birth. We conducted observational analyses within the water, sanitation, and hygiene (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 mo, including C-reactive protein (CRP), alpha-1-acid glycoprotein (AGP), and 13 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 prespecified. 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 mo, 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 of 28 mo, maternal RBP was positively associated with IFN-γ in children (0.07 [0.01, 0.14]), whereas maternal vitamin A deficiency was negatively associated with child AGP (-0.07 [-0.13, -0.02]). Maternal iron deficiency was associated with higher AGP concentrations in children at age 14 mo (0.13 [0.04, 0.23]), and maternal sTfR concentrations were positively associated with child CRP concentrations at age 28 mo (0.18 [0, 0.36]). Maternal deficiencies in vitamin A or iron during the first 2 trimesters of pregnancy may shape the trajectory of a child's immune status.

Sections du résumé

Background UNASSIGNED
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.
Objectives UNASSIGNED
We aimed to evaluate whether maternal micronutrients, stress, estriol, and immune status during the first or second trimester of pregnancy were associated with child immune status in the first two years after birth.
Methods UNASSIGNED
We conducted observational analyses within the water, sanitation, and hygiene (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 mo, including C-reactive protein (CRP), alpha-1-acid glycoprotein (AGP), and 13 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 prespecified. We used generalized additive models and reported the mean difference and 95% confidence intervals at the 25th and 75th percentiles of exposure distribution.
Results UNASSIGNED
At child age 14 mo, 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 of 28 mo, maternal RBP was positively associated with IFN-γ in children (0.07 [0.01, 0.14]), whereas maternal vitamin A deficiency was negatively associated with child AGP (-0.07 [-0.13, -0.02]). Maternal iron deficiency was associated with higher AGP concentrations in children at age 14 mo (0.13 [0.04, 0.23]), and maternal sTfR concentrations were positively associated with child CRP concentrations at age 28 mo (0.18 [0, 0.36]).
Conclusion UNASSIGNED
Maternal deficiencies in vitamin A or iron during the first 2 trimesters of pregnancy may shape the trajectory of a child's immune status.

Identifiants

pubmed: 37560460
doi: 10.1016/j.cdnut.2023.101969
pii: S2475-2991(23)24792-7
pmc: PMC10407622
doi:

Types de publication

Journal Article

Langues

eng

Pagination

101969

Subventions

Organisme : NIAID NIH HHS
ID : K01 AI136885
Pays : United States

Informations de copyright

© 2023 The Authors.

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Auteurs

Da Kyung Jung (DK)

Division of Epidemiology and Biostatistics, School of Public Health, University of California Berkeley, Berkeley, CA, United States.

Sophia T Tan (ST)

Division of Infectious Diseases and Geographic Medicine, Stanford University, Stanford, CA, United States.

Caitlin Hemlock (C)

Division of Epidemiology and Biostatistics, School of Public Health, University of California Berkeley, Berkeley, CA, United States.

Andrew N Mertens (AN)

Division of Epidemiology and Biostatistics, School of Public Health, University of California Berkeley, Berkeley, CA, United States.

Christine P Stewart (CP)

Institute for Global Nutrition, University of California Davis, Davis, CA, United States.

Md Ziaur Rahman (MZ)

Environmental Interventions Unit, Infectious Diseases Division, icddr,b, Dhaka 1212, Bangladesh.

Shahjahan Ali (S)

Environmental Interventions Unit, Infectious Diseases Division, icddr,b, Dhaka 1212, Bangladesh.

Rubhana Raqib (R)

Environmental Interventions Unit, Infectious Diseases Division, icddr,b, Dhaka 1212, Bangladesh.

Jessica A Grembi (JA)

Division of Infectious Diseases and Geographic Medicine, Stanford University, Stanford, CA, United States.

Mohammed Rabiul Karim (MR)

Environmental Interventions Unit, Infectious Diseases Division, icddr,b, Dhaka 1212, Bangladesh.

Sunny Shahriar (S)

Environmental Interventions Unit, Infectious Diseases Division, icddr,b, Dhaka 1212, Bangladesh.

Anjan Kumar Roy (AK)

Environmental Interventions Unit, Infectious Diseases Division, icddr,b, Dhaka 1212, Bangladesh.

Sarah Abdelrahman (S)

Division of Epidemiology and Biostatistics, School of Public Health, University of California Berkeley, Berkeley, CA, United States.

Abul K Shoab (AK)

Environmental Interventions Unit, Infectious Diseases Division, icddr,b, Dhaka 1212, Bangladesh.

Syeda L Famida (SL)

Environmental Interventions Unit, Infectious Diseases Division, icddr,b, Dhaka 1212, Bangladesh.

Md Saheen Hossen (MS)

Environmental Interventions Unit, Infectious Diseases Division, icddr,b, Dhaka 1212, Bangladesh.

Palash Mutsuddi (P)

Environmental Interventions Unit, Infectious Diseases Division, icddr,b, Dhaka 1212, Bangladesh.

Salma Akther (S)

Environmental Interventions Unit, Infectious Diseases Division, icddr,b, Dhaka 1212, Bangladesh.

Mahbubur Rahman (M)

Environmental Interventions Unit, Infectious Diseases Division, icddr,b, Dhaka 1212, Bangladesh.

Leanne Unicomb (L)

Environmental Interventions Unit, Infectious Diseases Division, icddr,b, Dhaka 1212, Bangladesh.

Lisa Hester (L)

Department of Medicine, University of Maryland, Baltimore, MD USA.

Douglas A Granger (DA)

Institute for Interdisciplinary Salivary Bioscience Research, University of California Irvine, Irvine, CA, United States.

Juergen Erhardt (J)

VitMin Lab, Willstätt, Germany.

Ruchira Tabassum Naved (RT)

Health System and Population Studies Division, icddr,b, Dhaka, Bangladesh.

Md Mahfuz Al Mamun (MM)

Health System and Population Studies Division, icddr,b, Dhaka, Bangladesh.

Kausar Parvin (K)

Health System and Population Studies Division, icddr,b, Dhaka, Bangladesh.

John M Colford (JM)

Division of Epidemiology and Biostatistics, School of Public Health, University of California Berkeley, Berkeley, CA, United States.

Lia C H Fernald (LCH)

Division of Community Health Sciences, School of Public Health, University of California, Berkeley, Berkeley, CA, United States.

Stephen P Luby (SP)

Division of Infectious Diseases and Geographic Medicine, Stanford University, Stanford, CA, United States.

Firdaus S Dhabhar (FS)

Department of Psychiatry & Behavioral Sciences, Department of Microbiology and Immunology, Sylvester Comprehensive Cancer Center, Miller School of Medicine, University of Miami, Miami, FL, United States.

Audrie Lin (A)

Department of Microbiology and Environmental Toxicology, University of California, Santa Cruz, CA, United States.

Classifications MeSH