BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
Authors: Daniel J Jackson; Michael D Evans; Ronald E Gangnon; Christopher J Tisler; Tressa E Pappas; Wai-Ming Lee; James E Gern; Robert F Lemanske Journal: Am J Respir Crit Care Med Date: 2011-09-29 Impact factor: 21.405
Authors: Dhara A Patel; Yingjian You; Guangming Huang; Derek E Byers; Hyun Jik Kim; Eugene Agapov; Martin L Moore; R Stokes Peebles; Mario Castro; Kaharu Sumino; Adrian Shifren; Steven L Brody; Michael J Holtzman Journal: J Allergy Clin Immunol Date: 2014-09-09 Impact factor: 10.793