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1 Lung and Allergy Research, Division of Physiology, Institute of Environmental Medicine, Karolinska Institute, and 2 National Institute for Working Life, Stockholm, Sweden.
CORRESPONDENCE: A. Ek, Lung and Allergy Research, Division of Physiology, Institute of Environmental Medicine, Karolinska Institutet, PO Box 287, SE-171 77, Stockholm, Sweden. Fax: 46 8300619. E-mail: alexandra.ek@imm.ki.se
Keywords: Bronchial responsiveness, corticosteroids, cytokines, nasal lavage, plasma proteins, serum
Received: February 13, 2004
Accepted May 12, 2004
This study was supported by Glaxo Smith Kline (Greenford, UK) and the Swedish Council for Work Life Research, the Swedish Farmers' Foundation for Agricultural Research, the Swedish Heart Lung Foundation and the Karolinska Institute (all Stockholm, Sweden).
Exposure to organic dust in a swine house causes acute airway inflammation and increased bronchial responsiveness to methacholine in healthy subjects. The aim of this study was to investigate whether an inhaled glucocorticoid, fluticasone propionate, alters the acute airway responses induced by exposure in a swine barn.
In 15 healthy subjects, analysis of nasal lavage fluids, serum samples and bronchial methacholine responsiveness were performed before and after exposure to organic dust in a swine house for 3 h. Seven subjects received fluticasone propionate (500 µg b.i.d. by inhalation and 100 µg intranasally once daily) and eight subjects received placebo during the 2 weeks prior to exposure.
Post-exposure plasma interleukin (IL)-6 levels and body temperature were significantly lower in the fluticasone group than in the placebo group. Intranasally administered fluticasone propionate significantly attenuated the plasma protein (assessed as albumin concentrations) leakage and IL-8 and tumour necrosis factor-
In conclusion, glucocorticoid treatment attenuated the inflammatory response to inhaled organic dust without influencing the increased bronchial responsiveness to methacholine.
response induced by exposure. Fluticasone propionate inhalation exerted no influence on the increased bronchial responsiveness to methacholine induced by exposure.
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