title: Identification of basophils by immunohistochemistry in the airways of post-mortem cases of fatal asthma.
abstract: There is increasing evidence for the role of basophils in the pathogenesis of bronchial asthma. To examine the presence of basophils in the airways of patients with fatal asthma by immunohistochemistry, we stained lung tissues from four post-mortem cases who had died from severe asthmatic attacks and four controls with a monoclonal antibody raised against tryptase (AA-1) and anti-IgE. Mast cells and basophils were identified in the bronchioles as AA-1- and anti-IgE-positive cells, and anti-IgE-positive cells, respectively. Airway mast cells were found beneath the basement membrane, near blood vessels in the submucosa, and adjacent to the submucosal glands, and scattered throughout the muscle bundles. There was a significant increase of mast cells in the asthma group compared with the control group (203.5+/-84.6/mm2, mean+/-s.d. vs 37.7+/-8.7/mm2, P<0.05, n=4). In contrast, basophils were observed in the airway lumen, in the bronchial epithelium and in the submucosa. The number of basophils in the bronchioles was 81.8+/-55.5/mm2 (n = 4); however, basophils were not found at all in the airways of the control group. Although eosinophils, B lymphocytes and macrophages bear low affinity IgE receptors and could react with anti-IgE, the location of these cells in the close sections did not correspond closely with basophils. The presence of basophils in lung tissues obtained from fatal asthma patients supports the view that basophils play a role in the pathogenesis of bronchial asthma.
authors.affiliation: Department of Medicine and Physical Therapy, Faculty of Medicine, University of Tokyo, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Koshino
authors.forename: S
authors.initials: S
authors.lastname: Teshima
authors.forename: N
authors.initials: N
authors.lastname: Fukushima
authors.forename: T
authors.initials: T
authors.lastname: Takaishi
authors.forename: K
authors.initials: K
authors.lastname: Hirai
authors.forename: Y
authors.initials: Y
authors.lastname: Miyamoto
authors.forename: Y
authors.initials: Y
authors.lastname: Arai
authors.forename: Y
authors.initials: Y
authors.lastname: Sano
authors.forename: K
authors.initials: K
authors.lastname: Ito
authors.forename: Y
authors.initials: Y
authors.lastname: Morita
mesh_terms: D000328:Adult; D000888:Antibodies, Anti-Idiotypic / Q000032:analysis; D000911:Antibodies, Monoclonal / Q000276:immunology; D001249:Asthma / Q000473:pathology*; D001485:Basement Membrane / Q000473:pathology; D001491:Basophils / Q000737:chemistry* / Q000473:pathology; D015415:Biomarkers; D001980:Bronchi / Q000737:chemistry / Q000473:pathology*; D000001:Calcimycin / Q000494:pharmacology; D020013:Calcium Signaling / Q000187:drug effects; D002478:Cells, Cultured; D002648:Child; D053818:Chymases; D004396:Coloring Agents; D005260:Female; D006801:Humans; D007124:Immunoenzyme Techniques; D007476:Ionophores / Q000494:pharmacology; D008168:Lung / Q000737:chemistry / Q000473:pathology*; D008297:Male; D008407:Mast Cells / Q000737:chemistry / Q000187:drug effects / Q000473:pathology; D008875:Middle Aged; D009092:Mucous Membrane / Q000473:pathology; D017455:Receptors, IgE / Q000276:immunology; D012697:Serine Endopeptidases / Q000032:analysis; D014048:Tolonium Chloride; D053802:Tryptases
chemical_list: D000888:Antibodies, Anti-Idiotypic; D000911:Antibodies, Monoclonal; D015415:Biomarkers; D004396:Coloring Agents; D007476:Ionophores; D017455:Receptors, IgE; C026408:anti-IgE antibodies; D014048:Tolonium Chloride; D000001:Calcimycin; D012697:Serine Endopeptidases; C083294:chymase 2; D053818:Chymases; D053802:Tryptases