Maternal immune status in pregnancy is related to offspring's immune responses and atopy risk
1Department of Environmental Immunology, UFZ, Helmholtz Centre for Environmental Research Leipzig, Germany.
Insights
Maternal immune responses during pregnancy influence infant immunity. Maternal IgE predicts infant IgE, and maternal atopic dermatitis (AD) is linked to childhood AD, but not inflammatory cytokines.
Area of Science:
- Immunology
- Pediatrics
- Allergy Research
Background:
- Maternal immune system influence on child's immune competence is not well understood.
- Pregnancy immune responses may impact atopic disease development.
- Prospective birth cohort study to analyze mother-child immune responses.
Purpose of the Study:
- Investigate maternal immune system effects on children's immune maturation.
- Determine links between maternal immune responses and childhood disease risks.
- Analyze cytokine and IgE levels in mother-child pairs.
Main Methods:
- Prospective birth cohort study (LINA study) with 353 mother-child pairs.
- Measured Th1/Th2/Th17, inflammatory cytokines/chemokines, and IgE in maternal blood (34th week gestation) and cord/1-year-old children's blood.
- Collected atopic outcome data via questionnaires.
Main Results:
- Cord blood had higher inflammatory markers than maternal blood.
- Infants showed lower Th1/Th2 cytokines with a Th2 bias at birth.
- Maternal inflammatory markers (MCP-1, IL-10, TNF-α) correlated with children's levels at age one.
- High maternal IgE associated with higher infant IgE; maternal AD linked to childhood AD.
Conclusions:
- Maternal inflammatory cytokines correlate with children's levels at age one, but not IgE or AD.
- Maternal IgE predicts infant IgE.
- Childhood atopic dermatitis is associated with maternal disease.
Background:
The influence of maternal immune responses in pregnancy on children's immune competence and the development of atopic diseases later in life are poorly understood. To determine potential maternal effects on the maturation of children's immune system and resulting disease risks, we analysed immune responses in mother-child pairs in a prospective birth cohort study.
Methods:
Within the Lifestyle and Environmental factors and their Influence on Newborns Allergy risk (LINA) study, concentrations of Th1/Th2/Th17 and inflammatory cytokines/chemokines as well as IgE were measured in phytohemagglutinin and lipopolysaccharide stimulated maternal blood in the 34th week of gestation and in corresponding children's blood at birth and 1 year after (n = 353 mother-child pairs). Information on atopic outcomes during the first year of life was obtained from questionnaires.
Results:
Concentrations of inflammatory markers, excepting TNF-α, were manifold higher in cord blood samples compared with maternal blood. Th1/Th2 cytokines were lower in children's blood with a Th2 bias at birth. Maternal inflammatory parameters (MCP-1, IL-10, TNF-α) in pregnancy showed an association with corresponding cytokines blood levels in children at the age of one. High maternal IgE concentrations in pregnancy were associated with increased children's IgE at birth and at the age of one, whereas children's atopic dermatitis (AD) was determined by maternal AD.
Conclusions:
Maternal inflammatory cytokines during pregnancy correlate with children's corresponding cytokines at the age of one but are not related to IgE or AD. While maternal IgE predicts children's IgE, AD in children is only associated with maternal disease.
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