title: Increased number of activated lymphocytes in human lung following swine dust inhalation.
abstract: Inhalation of swine dust causes intense alveolar inflammation, with recruitment of inflammatory cells, predominantly neutrophils, but also alveolar macrophages and lymphocytes. The present study focuses on the lymphocyte response to inhaled swine dust. Twenty four healthy, nonsmoking, nonallergic subjects were exposed to swine dust for 3 h in a swine confinement building. Bronchoalveolar lavage (BAL) was performed before and 24 h after the start of exposure, and blood samples were drawn before, and at 7 and 24 h after exposure. Total and differential cell counts were carried out. Monoclonal antibodies recognizing T-cells, T-cell subsets, T-cell activation markers, and B-cells were analysed by flow cytometry. The number of granulocytes increased more than 50 times and alveolar macrophages and lymphocytes increased two- to three-fold in BAL fluid. The exposure did not alter the proportion of T-cells but increased the number of activated T-cells in BAL fluid. The interleukin-2 (IL-2) receptor (CD25), human leucocyte antigen-DR (HLA-DR) major histocompatibility complex (MHC) class II and the early activation marker CD69 were expressed by 8.4% (25-75th percentiles 6.4-9.6%), 9.9% (8.2-21.6%) and 22.0% (18.1-24.3%) of the lymphocytes prior to exposure, and 11.6% (9.0-16.4%) (p < 0.01), 18.8% (12.9-30.4%) (p < 0.01) and 42.1% (38.4-47.3%) (p < 0.05), respectively, after the exposure. In peripheral blood, the concentration of T-cells decreased after exposure and B-cells increased slightly but significantly. The ratio naive/memory T-cells (CD45RA/RO) did not change in blood. In conclusion, 3 h of swine dust inhalation led to an influx of lymphocytes into the lower airways and increased expression of lymphocyte activation markers on the cell surface in previously unexposed subjects. The finding suggests a role for T-cells, in conjunction with other cells, in the inflammatory response to inhaled swine dust.
authors.affiliation: Dept of Occupational Health, National Institute for Working Life, Solna, Sweden.
authors.forename: C
authors.initials: C
authors.lastname: Müller-Suur
authors.forename: K
authors.initials: K
authors.lastname: Larsson
authors.forename: P
authors.initials: P
authors.lastname: Malmberg
authors.forename: P H
authors.initials: PH
authors.lastname: Larsson
mesh_terms: D000328:Adult; D000485:Allergens; D000818:Animals; D015703:Antigens, CD / Q000097:blood; D000945:Antigens, Differentiation, T-Lymphocyte / Q000097:blood; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology; D004391:Dust / Q000009:adverse effects*; D005260:Female; D006098:Granulocytes; D006684:HLA-DR Antigens / Q000097:blood; D000949:Histocompatibility Antigens Class II / Q000097:blood; D006801:Humans; D037181:Lectins, C-Type; D007958:Leukocyte Count; D008168:Lung / Q000276:immunology* / Q000473:pathology; D008213:Lymphocyte Activation; D018655:Lymphocyte Count; D016131:Lymphocyte Subsets; D008297:Male; D008875:Middle Aged; D015375:Receptors, Interleukin-2 / Q000097:blood; D013552:Swine; D000099192:CD69 Antigens
chemical_list: D000485:Allergens; D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D004391:Dust; D006684:HLA-DR Antigens; D000949:Histocompatibility Antigens Class II; D037181:Lectins, C-Type; D015375:Receptors, Interleukin-2; D000099192:CD69 Antigens