Antenatal determinants of neonatal immune responses to allergens.
BACKGROUND
The environmental factors responsible for recent increases in the prevalence of asthma and atopic disease have been assumed to act after birth. Their possible effects on fetal immune development in utero have not been investigated systematically, although sensitization to allergens may occur before birth.


OBJECTIVE
This prospective study determined whether the risk factors for asthma and atopic disease, namely family history of atopic disease, maternal smoking, birth order, or maternal dietary intake of antioxidant vitamins, exert antenatal effects on the fetal immune system that may predispose to childhood atopy.


METHODS
The T helper (Th) cell proliferative responses of cord blood mononuclear cells (CBMC) from a sample of 223 neonates, representative of children born to a cohort of 2000 pregnant women, were measured and related to family, maternal and environmental factors associated with the pregnancy.


RESULTS
The magnitude of CBMC-proliferative responses to allergens increased significantly in association with a family history of atopic disease or maternal smoking, and decreased significantly with increasing birth order and high maternal dietary intake of vitamin E. The epidemiological association between birth order and atopy may therefore be a consequence of antenatal influences rather than of protective effects of childhood infections. The association between maternal intake of vitamin E and CBMC responsiveness suggests that diet during pregnancy may influence the fetal immune system in such a way as to modulate the risk of childhood atopy.


CONCLUSIONS
These results provide a new insight into the aetiology of atopic disease by demonstrating that the maternal environmental risk factors for atopy, diet, birth order and smoking, influence the development of the fetal immune system. This raises the prospect of preventative public health interventions during pregnancy.
Devereux
G
G
Department of Environmental and Occupational Medicine, University Medical School, Aberdeen, Scotland, UK.
Barker
R N
RN
Seaton
A
A
D000485:Allergens / Q000276:immunology*; D000818:Animals; D000906:Antibodies / Q000276:immunology*; D000917:Antibody Formation; D001722:Birth Order; D002455:Cell Division; D015331:Cohort Studies; D004032:Diet; D004391:Dust; D005260:Female; D005312:Fetal Blood; D006801:Humans; D006967:Hypersensitivity / Q000209:etiology / Q000235:genetics / Q000276:immunology; D007231:Infant, Newborn; D008499:Medical Records; D008925:Mites / Q000276:immunology; D009000:Monocytes / Q000166:cytology; D009035:Mothers; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D011446:Prospective Studies; D012307:Risk Factors; D012907:Smoking / Q000009:adverse effects; D006377:T-Lymphocytes, Helper-Inducer / Q000166:cytology; D014810:Vitamin E / Q000008:administration & dosage
D000485:Allergens; D000906:Antibodies; D004391:Dust; D014810:Vitamin E