Total and antigen-specific Ige levels in umbilical cord blood

The present study was conducted to learn whether the perinatal and environmental factors could influence the total and antigen-specific IgE levels in umbilical cord blood. Retrospective data were obtained from 173 mother-infant pairs. Total and specific (for children's food, wheat/grass and house dust mite-HDM) cord blood IgE levels were determined using the immunoassay test. The total cord blood IgE was between 0.0-23.08 IU/ml (mean 0.55 ± 2.07 IU/ml; median 0.16 IU/ml). Total IgE levels were significantly higher in boys compared with girls (OR = 2.2; P = 0.007), and in newborns with complicated pregnancy (OR = 2.7; P = 0.003). A greater number of siblings correlated with increases in the total cord blood IgE (P < 0.02). We detected specific IgE in 34 newborns (40 positive tests). A long-standing contact with a cat during pregnancy decreased the specific IgE level for wheat/grass (OR = 3.2; P < 0.07) and for children's food (OR = 5.0; P < 0.04), and the contact with a dog decreased the specific-IgE for wheat/grass (OR = 0.3; P < 0.05). Exposure to tobacco smoke correlated with the positive specific IgE toward house dust mite (OR = 4.7; P = 0.005)

Prediction of atopy in the first year of life using cord blood IgE levels and family history

<p>Abstract</p> <p>We assessed correlations of total and specific cord-blood IgE (cIgE) levels with allergic symptoms in the first year of life. cIgE levels were determined by an immunoassay test in full-term neonates. This is a prospective study in which a questionnaire was used after birth, and at 6 and 12 months of age. We used multiple logistic regression models to assess the association between the family history of atopy and the incidence of allergy. The infants were divided in to groups based on the cIgE level (Group 1 < 0.1 IU/ml, n = 65; Group 2 0.1-0.5 IU/ml, n = 63; Group 3 > 0.5 IU/ml, n = 45). We found the symptoms of atopy in 26 children in Group 1 (40%), 30 (47.6%) in Group 2, and 17 (37.7%) in Group 3; the percentage of atopic diseases was in significantly different among the three groups. No association between a high total cIgE and specific cIgE with atopy family history and the outcome of atopic diseases was discovered. We conclude that neither total nor specific cIgE level with atopy family history can be used as an indicator to single out high risk infants.</p

High Fat Diet Inhibits Dendritic Cell and T Cell Response to Allergens but Does Not Impair Inhalational Respiratory Tolerance

<div><p>The incidence of obesity has risen to epidemic proportions in recent decades, most commonly attributed to an increasingly sedentary lifestyle, and a ‘western’ diet high in fat and low in fibre. Although non-allergic asthma is a well-established co-morbidity of obesity, the influence of obesity on allergic asthma is still under debate. Allergic asthma is thought to result from impaired tolerance to airborne antigens, so-called respiratory tolerance. We sought to investigate whether a diet high in fats affects the development of respiratory tolerance. Mice fed a high fat diet (HFD) for 8 weeks showed weight gain, metabolic disease, and alteration in gut microbiota, metabolites and glucose metabolism compared to age-matched mice fed normal chow diet (ND). Respiratory tolerance was induced by repeated intranasal (i.n.) administration of ovalbumin (OVA), prior to induction of allergic airway inflammation (AAI) by sensitization with OVA in alum i.p. and subsequent i.n. OVA challenge. Surprisingly, respiratory tolerance was induced equally well in HFD and ND mice, as evidenced by decreased lung eosinophilia and serum OVA-specific IgE production. However, in a pilot study, HFD mice showed a tendency for impaired activation of airway dendritic cells and regulatory T cells compared with ND mice after induction of respiratory tolerance. Moreover, the capacity of lymph node cells to produce IL-5 and IL-13 after AAI was drastically diminished in HFD mice compared to ND mice. These results indicate that HFD does not affect the inflammatory or B cell response to an allergen, but inhibits priming of Th2 cells and possibly dendritic cell and regulatory T cell activation.</p></div