Atopic phenotype in children is associated with decreased virus-induced interferon-alpha release

Interferon-alpha (IFN-alpha) production in humans is an early event in the nonspecific cellular response to viruses and mediates a wide range of antiviral and immunoregulatory activities. Little is known about the role of IFN-alpha in allergic disease.

In the present study, we performed a retrospective comparative analysis of 88 children with and without an atopic phenotype for virus-induced IFN-alpha production in blood cultures.

We were able to demonstrate that patients with allergic asthma (aA) produced significantly lower amounts of virus-induced IFN-alpha than healthy children and patients with nonallergic asthma (naA). Furthermore, the number of eosinophils in atopic children as a marker for allergic inflammation correlated negatively with the IFN-alpha level in blood cultures. Additionally, we found differences between aA and naA patients with respect to the capacity to produce IFN-gamma. Although atopy is thought to be associated with a Th2 cytokine response, in our study, IFN-gamma release was not reduced in the allergic children. In contrast, patients with allergic rhinitis showed a significant increase in IFN-gamma release compared to naA patients.

In our study, an early atopic phenotype was related to a reduction in virus induced IFN-alpha release from blood cultures. Thus, after further prospective evaluation, the IFN-alpha level may serve as an additional in vitro marker for the definition of atopy in children.