Fetal and neonatal IL-13 production during pregnancy and at birth and subsequent development of atopic symptoms.
BACKGROUND
Cytokine production at the materno-fetal interface may influence the development of atopy-predisposing immune responses. Because IL-13 possesses IL-4-like activity and may regulate the immune responses observed in atopy, it may contribute to the expression of the atopic phenotype initiated during intrauterine life.


OBJECTIVE
We sought to examine IL-13 expression by fetal and neonatal cells and the placenta.


METHODS
The production of IL-13 by neonatal and fetal T cells was examined by culturing the cells in the presence or absence of PHA. Production of IL-13 at term was considered in the context of the later development of atopic disease in the child. IL-13 expression in the placenta was assessed by using immunohistochemistry.


RESULTS
IL-13 immunoreactivity within the placenta was restricted to 16 to 27 weeks' gestation (6/6 positive vs 0/10 at >27 weeks' gestation). In contrast, spontaneous release of IL-13 by fetal mononuclear cells was first observed from 27 weeks' gestation but was undetectable after 37 weeks' gestation. PHA-stimulated mononuclear cells showed increased IL-13 levels in 80% of samples. Term babies (>37 weeks' gestation) with a parental history of atopy with atopic symptoms by 3 years of age produced significantly lower concentrations of PHA-induced IL-13 when compared with babies with no parental history of atopy (P =.034).


CONCLUSIONS
Thus babies at risk of atopic disease in infancy display defective IL-13 production at birth. This may represent an inherent immaturity in the development of T cell-cytokine responses in babies at genetic risk for atopy or could be a consequence of downregulation of responses by other factors. Normal pregnancy, irrespective of atopic status, is associated with the production of appreciable quantities of IL-13 initially by the placenta and subsequently by the fetus. The regulation of this production and its consequences for the mother and fetus remains to be elaborated.
Williams
T J
TJ
Child Health, School of Medicine, University of Southampton, UK.
Jones
C A
CA
Miles
E A
EA
Warner
J O
JO
Warner
J A
JA
D005260:Female; D005312:Fetal Blood / Q000737:chemistry; D005333:Fetus / Q000378:metabolism*; D005865:Gestational Age; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000097:blood / Q000276:immunology / Q000378:metabolism*; D007231:Infant, Newborn; D018793:Interleukin-13 / Q000096:biosynthesis*; D007743:Labor, Obstetric / Q000097:blood / Q000378:metabolism*; D007963:Leukocytes, Mononuclear / Q000737:chemistry; D010920:Placenta / Q000378:metabolism; D011247:Pregnancy / Q000097:blood / Q000378:metabolism*
D018793:Interleukin-13