title: IgE and the allergy-asthma connection in the 23-year follow-up of Brown University students.
abstract: The Hygiene Hypothesis helps to explain the increased epidemiology of atopy, especially asthma and hay fever. This hypothesis depends on two major immunological pathways, the Th1 and the Th2 pathways, which are mutually inhibitory, with the Th2 pathway being the dominant one in fetal life and the newborn. The Th1 leads to a cellular delayed hypersensitive response while the Th2 pathway leads to increased IgE, eosinophilia, atopy, and airway/hyperresponsiveness. The ever-increasing vaccines for immunization against viral and bacterial microorganisms together with better public health hygiene procedures introduce a bias in favor of the inhibition of the Th1 pathway, thereby allowing the Th2 pathway, with its IgE hypersensitivity, to predominate. We have attempted to correlate this new hypothesis with data from our Brown University college student longitudinal study. In this study, our data have demonstrated that allergen sensitization (positive pollen skin tests reactions) leads to an increased risk factor for developing asthma. Most of our asthmatic patients in our longitudinal study had positive allergy skin tests. Also, students born in months with high concentrations of atmospheric ragweed pollen had an increased risk of developing sensitization to ragweed and later to develop hay fever, which may lead to asthma. There is a strong association of asthma with hay fever (a classic IgE disease). Also, hay fever patients have three times the risk for developing asthma than controls. There appear to be several factors needed to express the phenotype of allergic asthma: elevated IgE, eosinophilia, airway hyperresponsiveness, exposure to allergens, and the predominance of the Th2 pathway of immunologic reactions.
authors.affiliation: Brown University School of Medicine, Providence, Rhode Island 02906, USA.
authors.forename: R J
authors.initials: RJ
authors.lastname: Settipane
authors.forename: G A
authors.initials: GA
authors.lastname: Settipane
mesh_terms: D000485:Allergens / Q000009:adverse effects; D001249:Asthma / Q000209:etiology / Q000276:immunology*; D015331:Cohort Studies; D004802:Eosinophilia / Q000276:immunology; D006801:Humans; D006967:Hypersensitivity / Q000209:etiology / Q000276:immunology*; D007114:Immunization; D007073:Immunoglobulin E / Q000276:immunology*; D011058:Pollen / Q000009:adverse effects; D006255:Rhinitis, Allergic, Seasonal / Q000276:immunology; D012307:Risk Factors; D012882:Skin Tests; D013334:Students; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology; D014611:Vaccination / Q000009:adverse effects
chemical_list: D000485:Allergens; D007073:Immunoglobulin E