| Summary: | Background: Epigenetic control of gene expression profiles is a ubiquitous mechanism during cell differentiation, organogenesis and chronic inflammatory reactions. Recent studies have shown that allergen exposure during very early pregnancy increases bronchial hypersensitivity in offspring in a murine model of bronchial asthma. However, no such phenomena were reported in humans. In the present study, the role of epigenetic control in the onset of allergic diseases was investigated.
Methods: A total of 400 pairs of mothers with physician-diagnosed allergic rhinitis (AR) and their offspring (age 7-18 months) who participated in a large-scale medical check-up were enrolled in this retrospective cohort study. Family history of allergic diseases and the presence or absence of AR symptoms during pregnancy were inquired about using a self-answered questionnaire. A logistic regression model adjusted for age, gender, birth month and father's history of allergic diseases was statistically analyzed.
Results: Offspring whose mothers had any AR symptoms during early pregnancy showed a significantly higher adjusted odds ratio for the onset of AR in offspring than those whose mothers had no symptoms during pregnancy (adjusted Odds Ratio: 6.26, p=0.036). However, the symptoms of AR during late pregnancy showed no effects on the odds ratio. In contrast, the presence or absence of AR symptoms during early or late pregnancy showed no association with the prevalence of food allergy, atopic dermatitis or asthma in offspring. Conclusions: Our results suggest the presence of possible epigenetic mechanisms regulating the onset of AR in humans presumably through increased organ-specific hypersensitivity.
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