Production of interleukin 4 and interferon gamma in CD8+ T cells from patients with intrinsic and extrinsic asthma / 천식및알레르기

BACKGROUND: Asthma has been divided clinically into extrinsic and intrinsic variants. However, it is not clear whether these two types of clinically different asthma are mediated by immunolo- gically common pathogenesis or not. Recently, the role of CD8+ T cells in allergic inflammation was suggested. OBJECTIVES: The aims of this study were to determine the role of CD8+ T cells in asthma through the production of interleukin 4 (IL-4) and interferon gamma (IFN-gamma), and to see if there were any differences in cytokine production in CD8+ T cell by the two clinically different asthma types, intrinsic and extrinsic asthma. METHOD: Peripheral blood mononuclear cells from intrinsic and extrinsic asthmatic patients and from healthy subjects were cultured and stimulated with phorbol ester and calcium ionophore. A three-color flow cytometric analysis was used for IL-4 and IFN-gamma detection in CD8+ T cells. RESULTS: Intracytoplasmic IL-4 and IFN-gamma positive CD8+ T cells were significantly higher in asthmatic patients compared to normal subjects. However, there were no significant differences of IL-4 and IFN-gamma production between intrinsic and extrinsic asthmatic patients (IL-4:12.5+/-4.2% in intrinsic asthmatics, 16.3+/-7.2% in extrinsic asthmatics, 4.2+/-2.1% in normals; IFN-gamma: 33.4+/-3.2%, 35.4+/-5.5%, 25.3+/-9.8%, respectively) CONCLUSION: These results suggest that intrinsic and extrinsic asthma have common immuno- pathogenesis and CD8+ T cells seem to participate in asthmatic inflammation by producing IL-4 and IFN-gamma.

Pervalence of sensiticity to aspirin (ASA) and food additives in subjects diagnosed as having intrinsic asthma / 천식및알레르기

Objective and METHOD: In order to identify the aggravating agents for intrinsic asthma, we performed ASA- and food additive-challenge tests on 182 subjects diagnosed as having intrinsic asthma. The following tests were performed: Lysine-aspirin bronchoprovocation test to confirm aspirin-sensitivity, sodium bi-sulfite (40-200mg) oral provocation test for sulfite sensitivity, tartrazine oral provocation test (50mg) for tartrazine sensitivity, and sodium benzoate (400mg) oral provocation test for sodium benzoate sensitivity. Positive reaction was defined as decrease in FEV, by more than 20% from the baseline value after the provocation. RESULT: Seventy-five (41.2%) of 182 subjects showed positive responses to more than one agent among the aspirin and three food additives challenged. The prevalence of aspirin-sensitivity was the highest (22.5%), followed by sulfite-sensitivity (8.8%), and then concurrent sensitivity to both aspirin and sulfite (6.0% ), to both aspirin and tartrazine (1.6% ), to aspirin, sulfite and tartrazine (1.1%) and to aspirin, sulfite and sodium benzoate (0.5%). Rhino-sinusitis was noted in 62.5% of aspirin-sensitive asthmatic subjects, 60% of sulfite-sensitive ones, and 80% of tartrazine-sensitive ones. Urticaria was noted in 21.4% of aspirin-sensitive asthmatic subjects, 16.6% of sulfite-sensitive ones and 6.3% of tartrazine-sensitive ones. Thirty-seven to 83% of positive responders had no adverse reaction history. CONCLUSION: These findings suggest that ASA and food additive challenge tests should be considered as a screening test to evaluate any aggravating factors in subjects with intrinsic asthma, even though they may not have experienced any adverse reactions.

Asma y deficiencia de subclases de IgG / Asthma and IgG subclasses deficiency

Se estudiaron 45 pacientes asmáticos adultos de difícil manejo, de más de 5 años de evolución, 37 de ellos esteroide dependientes y 8 no dependientes, con asma alérgica o intrínseca y algunos con infecciones respiratorias recurrentes de predominio viral. Por nefelometría se midieron los niveles séricos de las Igs G, M y A, y por ELISA se determinó la IgE total. Se encontraron 4 pacientes con deficiencia de IgG total, en el grupo de los esteroide dependientes. Mediante ELISA tlpo sandwich y con anticuerpos monoclonales específicos para las subclases de IgG se investigaron los niveles séricos de IgG1, 2, 3 y 4. En el 55.6 por ceinto de los enfermos se encontraron una O más deficiencias de subclases. No hubo diferencias significativas entre los grupos esteroide y no esteroide dependientes, ni entre los asmáticos alérgicos e intrínsecos, ni entre los con infección recurrente o sin ella. Predominó la deficiencia de IgG1; en total el 46.7 por ciento de los pacientes tenían deficiencia aislada o combinada de IgG1, el 31.1 por ciento de IgG2, el 24.4por ciento de IgG3 y el 17.8 por ciento de Igd4. La alta incidencia de deficiencia de subclases podría deberse a la acción de los esteroides o a una alteración en la regulación de la síntesis de Igs producida por un defecto Inmune primario. Esta deficiencia sería la responsable del comportamiento agresivo de la enfermedad

We studied 45 adult asthmatic patients with difficult to care disease and who had more than five years of evolution; they suffered from elther allergic or intrinsic asthma and some had experienced recurrent respiratory tract infections. predominantly of viral etiology. Serum levels of IgA, IgG and IgM were measured by nephelometry and total lgE was determined by an Enzyme-Linked immunosorbent Assay (ELISA). Total lgG deficiency was found in four steroid. dependent patients. Serum levels of IgG subclasses 1 to 4 were measured by means of a sandwich-like ELISA with specific monoclonal antibodies. One or more subclass deficiencies were present In 55.6% of the patients. Significant differences were not found between the following groups: steroid and nonsteroid dependent patients; allergic or intrinsic, asthma; and individuals with or without history of infection. IgG 1 deficiency was the most commonly found: It was present in 46.7% of the patients, either as an isolated disorder or combined with alteration of other subclasses. Deficiency of other subclasses was present in the following proportions: 31.1% for IgG2; 24.4% for IgG3 and 17.8 for IgG4. The high incidence of subclass deficiency may be due to steroid action or to primary Immune defects leading to disorders of IgG synthesis. Such situation might be responsible for the aggressive behavior of the disease