title: NIH conference. Asthma.
abstract: Asthma is characterized by inflammation, reversible airway obstruction, and increased airway responsiveness to various stimuli. It has received wide public attention in recent years because of increasing morbidity and deaths, particularly among black persons. The important role of inflammation in the immunopathogenesis of asthma has led to a newer therapeutic approach directed at interrupting this inflammatory process. Among immune regulatory pathways involved in asthma pathogenesis, two lymphokines appear to be particularly important in controlling IgE production. Interleukin-4 is required for IgE production; without it, IgE production is inhibited. Interferon-gamma can diminish cell priming for interleukin-4 production. Thus, the interplay of these two cytokines will determine whether cells that can make interleukin-4 will be produced and, therefore, whether IgE will be produced in response to allergic stimuli. Further, in response to appropriate stimuli, mast cells and eosinophils are attracted to airways and release cytokines, lipid mediators, and preformed substances that cause inflammation. Modern asthma treatment is directed at interrupting this inflammatory process and places a much greater emphasis on use of anti-inflammatory agents, such as aerosolized or parenteral corticosteroids, and on non-steroidal anti-inflammatory agents, such as cromolyn sodium and nedocromil sodium. Research advances without therapeutic application, however, limit success. Projects such as the National Institute of Allergy and Infectious Diseases' National Cooperative Inner-City Asthma Study, which is directed toward underserved populations, are intended to identify more clearly the factors responsible for increasing morbidity and to develop appropriate therapeutic interventions.
authors.affiliation: National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.
authors.forename: R A
authors.initials: RA
authors.lastname: Goldstein
authors.forename: W E
authors.initials: WE
authors.lastname: Paul
authors.forename: D D
authors.initials: DD
authors.lastname: Metcalfe
authors.forename: W W
authors.initials: WW
authors.lastname: Busse
authors.forename: E R
authors.initials: ER
authors.lastname: Reece
mesh_terms: D001249:Asthma / Q000276:immunology / Q000503:physiopathology / Q000628:therapy; D006801:Humans; D014481:United States