title: Suppression of the immune system by oral glucocorticoid therapy in bronchial asthma.
abstract: The effect of systemic glucocorticoid therapy on immune parameters was studied in patients with bronchial asthma. Patients were divided into two groups: 1) those receiving oral glucocorticoid; 2) control patients who did not receive systemic glucocorticoid treatment. The glucocorticoid dose varied between 5 and 70 mg per day. Patients had been taking oral therapy for at least 1 year. Glucocorticoid treatment was associated with an increased frequency of respiratory tract infections. Therefore, we need to define immune parameters which may predict an increased risk of infections. In this study, we analyzed several surface markers on lymphocytes and monocytes by flow cytometry. A significant reduction of the ratio of peripheral blood CD4+ to CD8+ T cells was associated with the administration of oral glucocorticoids. Furthermore, the expression of the HLA-DR molecule on monocytes was reduced in patients with systemic glucocorticoid therapy compared to control patients. Moreover, the capacity to elaborate cytokines by peripheral blood mononuclear cells upon stimulation was greatly reduced after exposure to glucocorticoids in vivo and in vitro. In addition, the humoral immune response was affected, because reduced IgG, IgM, and IgA levels were observed in patients receiving oral glucocorticoids. These results indicate that systemic glucocorticoid treatment in patients with bronchial asthma is associated with cellular and humoral immunosuppression which results in an increased risk of bacterial and viral infections.
authors.affiliation: Swiss Institute of Allergy and Asthma Research (SIAF), University of Zurich, Davos, Switzerland.
authors.forename: A G
authors.initials: AG
authors.lastname: Oehling
authors.forename: C A
authors.initials: CA
authors.lastname: Akdis
authors.forename: A
authors.initials: A
authors.lastname: Schapowal
authors.forename: K
authors.initials: K
authors.lastname: Blaser
authors.forename: M
authors.initials: M
authors.lastname: Schmitz
authors.forename: H U
authors.initials: HU
authors.lastname: Simon
mesh_terms: D000284:Administration, Oral; D001249:Asthma / Q000188:drug therapy* / Q000453:epidemiology; D016516:CD4-CD8 Ratio / Q000187:drug effects; D002478:Cells, Cultured; D004198:Disease Susceptibility; D004334:Drug Administration Schedule; D004804:Eosinophils / Q000187:drug effects; D005260:Female; D005938:Glucocorticoids / Q000008:administration & dosage / Q000009:adverse effects*; D006684:HLA-DR Antigens / Q000096:biosynthesis; D006801:Humans; D007107:Immune System / Q000187:drug effects*; D007136:Immunoglobulins / Q000096:biosynthesis / Q000187:drug effects; D007166:Immunosuppressive Agents / Q000009:adverse effects*; D015994:Incidence; D007371:Interferon-gamma / Q000096:biosynthesis; D015847:Interleukin-4 / Q000096:biosynthesis; D015848:Interleukin-5 / Q000096:biosynthesis; D007958:Leukocyte Count / Q000187:drug effects; D018655:Lymphocyte Count / Q000187:drug effects; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology; D011241:Prednisone / Q000008:administration & dosage / Q000009:adverse effects*; D012189:Retrospective Studies
chemical_list: D005938:Glucocorticoids; D006684:HLA-DR Antigens; D007136:Immunoglobulins; D007166:Immunosuppressive Agents; D015848:Interleukin-5; D015847:Interleukin-4; D007371:Interferon-gamma; D011241:Prednisone