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• Cord blood allergen-specific IgE is associated with reduced cord blood IFN-γ production
• Asthma status alone increases susceptibility to serious pneumococcal disease
• Asthma, eczema, and cytokine responses following severe respiratory syncytial virus bronchiolitis
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Cord blood allergen-specific IgE is associated with reduced cord blood IFN-γ production 

Previous studies have shown that cord blood (CB) might contain measurable amounts of allergen-specific IgE antibodies. It is still unclear whether these antibodies are of maternal or fetal origin and related to the production of specific CB cytokines. As reported in this issue of the Journal, Pfefferle et al (p 711) investigated the relationship between allergen-specific cord blood IgE levels, parental sensitization, and CB cytokines in neonates recruited for the multicenter birth cohort PASTURE study, which features the allergy-protecting farming environment. Allergen-specific IgE antibodies were detectable in 23.9% of newborns, and contamination with maternal serum could be excluded by several lines of experiments. Concordance between CB IgE and maternal IgE against the same allergen was very low for inhalant allergens; the concordance for various food allergens was considerably higher, particularly for IgE against hen's egg, cow's milk, and soy bean (see Figure). Particularly for seasonal allergens, approximately one half of the IgE-positive children had IgE-negative mothers. Neonatal IgE correlated negatively with the high levels of IFN-γ produced by CB mononuclear cells. These findings suggest that allergen-specific IgE antibodies detected in CB are most probably of fetal origin and that shaping of IgE antibody production might already take place in utero.

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• Significant inverse association between CB IgE and IFN-γ produced by CB mononuclear cells.

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Asthma status alone increases susceptibility to serious pneumococcal disease 

Juhn et al (p 719) report that adults with asthma are at an increased risk of developing serious pneumococcal disease (SPD), defined as an invasive pneumococcal disease and/or pneumococcal pneumonia, in comparison with those without asthma. They conducted a population-based case-control study in Rochester, Minn, during the primarily prepneumococcal vaccine era (1964 to 1983). The likelihood of SPD was almost 7 times higher among adults with asthma than among those without asthma, suggesting that asthma significantly increased risk for SPD. These results are consistent with the study findings recently reported by Talbot et al, who reported that both adults and children with asthma had an increased risk of invasive pneumococcal disease compared with those without asthma. Juhn et al also report that 17% of the burden of serious pneumococcal disease can be attributed to asthma status at a population level. The mechanisms underlying this increased risk of SPD among individuals with asthma require further study. In the meantime, consideration should be given to including asthma as an indication for pneumococcal vaccination in adults of all ages. Currently, the Advisory Committee of Immunization Practices does not recommend routine pneumococcal vaccinations for adults with asthma.

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Asthma, eczema, and cytokine responses following severe respiratory syncytial virus bronchiolitis 

Bronchiolitis due to respiratory syncytial virus (RSV) is a common antecedent to childhood asthma, a disorder associated with a T_H2 cytokine profile. As reported in this issue, Castro et al (p 726) examined patterns of cytokine production in a prospectively assembled cohort of 206 children after hospitalization for severe RSV bronchiolitis during the first year of life. By 6 years of age, both doctor-diagnosed asthma and eczema developed in almost one half of the children. Those who developed asthma had lower peripheral blood IL-13 expression at age 6 years than children without asthma. However, there were no differences in other cytokine levels (IL-2, IL-4, and IFN-γ). These data suggest that severe RSV infection is often followed by allergic sequelae and asthma, but, contrary to expectations, the immunologic development was not associated with a T_H2 phenotype in the peripheral blood. Newer immunologic approaches, including studying the response at the end-organ level and in different immune cell populations, are needed.