[Genesis of food allergy in infancy]. / Genèse de l'allergie alimentaire du nourrisson: possibilité d'une prophylaxie partielle.

Food allergy originates from physiological fetal Th2 polarization. The normal shift towards Th1 dominance during the first months of life is defective in the atopic infant. Several factors are critical for the development of food allergy. The influence of genetic factors has been shown by familial aggregation studies, and numerous candidate genes have been identified Gene polymorphisms interact with the environment, contributing to fetal programming Heritable epigenetic modifications occur rapidly in response to environmental factors and may explain the recent increase in food allergies and other atopic diseases. Atmospheric agents and the maternal diet during pregnancy may either increase or decrease the risk. Birth conditions, the intestinal microbiota, age at which food diversification begins, and exposure to food allergens and pollutants by inhalation, ingestion and skin contact may all contribute to the onset of food allergy in infancy. Partial prophylaxis is now within reach. Preventive information must be provided to families at high risk of atopy in their offspring.

Perception of dietary food items as food allergens in asthmatic individuals in north Indian population.

BACKGROUND AND OBJECTIVE: The role of food allergy in asthma is well recognized but is poorly quantified. The aim of the present study was to document perceived food items as allergens and to determine their association with age, sex, socioeconomic status (SES), family history of asthma, smoking history, duration of illness, and total serum immunoglobulin (Ig)E. METHODS: A total of 261 clinically and spirometrically diagnosed patients with asthma were included in this study on an accrual basis. Of these, 237 patients thought that their asthma became aggravated after consumption of at least 1 food item. The perceived food item allergy and its association with age, sex, SES, family history of asthma, smoking history, duration of illness, and total serum IgE were assessed using a detailed, open-ended questionnaire. RESULTS: Food items were perceived as main allergens by 90% (237/261) of responders. Sixty-five percent (154/237) of patients who perceived at least 1 food item as an allergen had high total serum IgE levels. Of 22 suspected food items, 16 were significantly (p < 0.05) associated with at least 1 of the 6 study parameters. CONCLUSION: Food items play a major role as food allergens on the basis of perception in asthmatic individuals. Some suspected food items are significantly associated with the demographic profile of asthmatic individuals.

Development and regulation of immune responses to food antigens in pre- and postnatal life.

Food antigens are harmless environmental components. The physiological response is the development of clinical and immunological tolerance. It is now well appreciated that tolerance development is the result of active immunoregulation and depends on a close interaction between the innate and adaptive immune system resulting in the development of tolerance-mediating T-cell responses. Programming of the immune system, particularly with regard to tolerance development, already starts before birth and stays under close control of the maternal immune system. Therefore, the pre-and postnatal period represents an important 'window of opportunity' for immunoprogramming. Underlying mechanisms include maternal cell transmission, antibody transfer, transfer of mediates/cytokines, and transmission of antigens and allergens. Immunoprogramming is fostered and augmented in the context of microbial components. Recently, several microbes have been identified which possess the capacity of immunoprogramming early in life. Epigenetic regulation represents an important novel mechanism in this regard. This concept opens new avenues for the development of preventive strategies to avoid inappropriate immune responses against food antigens.

Cord blood IgE against milk and egg antigens.

The aim of the present study was to reevaluate the prenatal production of specific IgE for eggs and milk and, in those cases, to determine whether there is a relation to the amount of maternal egg and milk intake. Total and specific IgEs from 160 cord blood-samples were determined by immunoassays using a paramagnetic particle solid phase and an enzyme-mediated chemiluminescent reaction for signal detection. The levels of cord blood IgE for total, egg, and milk were 0.63 +/- (SD) 1.10 IU/ml, 0.020 +/- 0.055, and 0.036 +/- 0.053 IU/ml, respectively. IgE levels specific to egg and milk over 0.03 IU/ml were observed in 33 and 70 out of 160 cases, respectively. To address whether the maternal intake of eggs and milk affects the level of cord blood IgEs, all mothers except 9 were interviewed, and the amount of eggs and milk taken during pregnancy was recorded. No correlation was seen between egg and milk intakes and cord blood IgE levels. Our data demonstrate a high incidence of the prenatal production of specific IgE for eggs and milk which is independent of maternal egg and milk intakes.