Search

Recently, immediate allergic reactions, including anaphylaxis, after Pachycondyla chinensis ant stings have been frequently reported in Korea. To estimate the prevalence of these reactions and the sensitization rate to P chinensis , we undertook a visit-questionnaire survey of the 327 adult residents living in a town in an ant-infested area in Korea. Skin prick tests with 6 common inhalant allergens, 3 bee venom allergens, and P chinensis whole body extract were performed on all ant-allergic subjects, on 86 asymptomatic residents, and on 37 controls outside the area. The serum-specific IgE to P chinensis extract was determined by ELISA. Seven subjects (2.1%) reported that they had experienced systemic allergic reactions to P chinensis stings; 4 of them had anaphylactic reactions. Large local reactions occurred in an additional 5 subjects (1.6%). All subjects with systemic allergic reactions had positive skin prick test results to P chinensis extract, whereas 23.3% of asymptomatic residents and 2.7% of the controls showed positive skin prick test results. The serum-specific IgE level was significantly higher in the subjects with systemic reactions than in the subjects with local reactions, the asymptomatic sensitizers, and the nonatopic controls. Sensitization to bee venom was found in 25% of the P chinensis -allergic subjects; this was significantly higher than the 3% rate seen in nonsensitized subjects. In conclusion, we report a 2.1% prevalence of systemic allergic reactions after P chinensis stings, based on self-reported symptoms, in an ant-infested area in Korea. (J Allergy Clin Immunol 2002;110:54-7.)

Background Respiratory syncytial virus (RSV)–specific IgE is a component of the host response to RSV infection, but its role in the subsequent enhancement of altered airway responsiveness is unknown. Objective To define the role of RSV-specific IgE in the enhancement of airway responsiveness on reinfection of newborn mice. Methods Mice were infected as newborns with RSV and were reinfected 5 weeks later. The role of IgE was determined by documenting RSV-specific IgE response after neonatal infection, and by assessing airway responsiveness on reinfection. Results After neonatal infection, wild-type (WT) mice developed an RSV-specific IgE response. On reinfection, these mice developed enhanced airway hyperresponsiveness (AHR), airway eosinophilia, and mucus hyperproduction, and their T-cell cytokine response was skewed toward a T H 2 phenotype. None of these altered responses developed on reinfection of IL-4 −/− /IL-13 −/− mice, and no RSV-specific IgE could be detected after neonatal infection of these mice. FcɛRI −/− mice did not develop the enhanced AHR on reinfection, and airway eosinophilia and mucus production were significantly attenuated. These responses could be restored in deficient mice reconstituted with WT mast cells. In RSV-infected newborn WT mice, administration of anti-IgE prevented the enhancement of AHR and attenuated eosinophilia and mucus hyperproduction on reinfection, an effect that was associated with diminished T H 2 cytokine production and increased IFN-γ production. Conclusion Respiratory syncytial virus–specific IgE enhances the development of T H 2-biased airway responsiveness on reinfection of mice initially infected as newborns.