Distinct Sex-Specific Gene Expression Changes in the Placenta in Association with Childhood Allergy

Astrud R Tuck

doi:10.23937/2378-3516/1410033

Abstract

Background: The prevalence of allergic disease has risen significantly during recent years. A major component of the susceptibility to allergic disease is determined in prenatal life, when the placenta plays a central role in fetal growth and development. In this study, we aimed to identify the patterns of gene expression in the placenta that may program early immune function to increase susceptibility to allergy. Methods: A set of immune genes known to be associated with asthma, allergy and inflammation were selected for analysis by quantitative real-time polymerase chain reaction (qRT-PCR) on placental tissue from infants who did or did not develop an allergy by 2 years of age. Analysis was performed on males and females separately for each allergy type including eczema, rhinitis or asthma. Results: Of 11 candidate allergy-associated genes tested by qRT-PCR, 4 were found to be associated with the development of specific childhood allergy types (P < 0.05). These included MMP9 for both males and females that developed eczema, TLR7 for females that developed eczema, KITL1 for males that developed rhinitis and ORMDL3 for females that developed asthma. Conclusions: This study has identified altered expression of placental genes involved in inflammation in association with the development of specific allergies in childhood. The current data provide supporting evidence implicating the placenta in programming the fetal immune system in early life.

Highlights

There has been an epidemic rise in allergic disease since the second-half of the twentieth century, in Western countries [1,2]
In particular there are significant differences in the placental immune response to the presence of maternal allergy [13] and its regulation by glucocorticoids between male and female placentae [14] with female placentae appearing more sensitive to an immune challenge and glucocorticoids relative to male placentae. These findings suggest that any placental immune dysregulation that leads to the susceptibility to allergy in later life may be vary in a sex specific manner
Some placental genes identified from the preliminary microarray work that were selected for analysis were not found to vary significantly in relation to allergic phenotype and so have been listed in table 2

Summary

Introduction

There has been an epidemic rise in allergic disease since the second-half of the twentieth century, in Western countries [1,2]. Diseases such as eczema, allergic rhinitis and food allergies represent significant burdens to human health. The placenta plays a central role in fetal growth and development and acts as the immunological and metabolic interface between the mother and fetus. A major component of the susceptibility to allergic disease is determined in prenatal life, when the placenta plays a central role in fetal growth and development. We aimed to identify the patterns of gene expression in the placenta that may program early immune function to increase susceptibility to allergy

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Results

Conclusion