title: Activated T-lymphocytes and eosinophils in the bronchial mucosa in isocyanate-induced asthma.
abstract: We have studied the phenotype and activation status of leukocytes in the bronchial mucosa in patients with isocyanate-induced asthma. Fiberoptic bronchial biopsy specimens were obtained from nine subjects with occupational (five toluene- and four methylene diisocyanate-sensitive) asthma, 10 subjects with extrinsic asthma, and 12 nonatopic healthy control subjects. Bronchial biopsy specimens were examined by immunohistology with a panel of monoclonal antibodies and the alkaline phosphatase-antialkaline phosphatase method. There was a significant increase in the number of CD25+ cells (interleukin-2 receptor-bearing cells, presumed "activated" T-lymphocytes; p less than 0.01) in isocyanate-induced asthma compared with that of control subjects. There were also significant increases in major basic protein (BMK-13)-positive (p less than 0.02) and EG2-positive (p less than 0.01) cells that represent total and "activated" eosinophil cationic protein-secreting eosinophils, respectively. In agreement with our previous findings, CD25+ (p less than 0.01), BMK-13 (p less than 0.03), and EG2+ (p less than 0.01) cells were also elevated in extrinsic asthma. No significant differences were observed in the numbers of T-lymphocyte phenotypic markers (CD3, CD4, and CD8) between subjects with asthma (isocyanate-induced and extrinsic) and control subjects. Similarly, no significant differences in immunostaining for neutrophil elastase (neutrophils) or CD68 (macrophages) were observed. The results suggest that isocyanate-induced occupational asthma and atopic (extrinsic) asthma have a similar pattern of inflammatory cell infiltrate. The results support the view that T-lymphocyte activation and eosinophil recruitment may be important in asthma of diverse etiology.
authors.affiliation: Department of Allergy and Clinical Immunology, National Heart & Lung Institute, London, England.
authors.forename: A M
authors.initials: AM
authors.lastname: Bentley
authors.forename: P
authors.initials: P
authors.lastname: Maestrelli
authors.forename: M
authors.initials: M
authors.lastname: Saetta
authors.forename: L M
authors.initials: LM
authors.lastname: Fabbri
authors.forename: D S
authors.initials: DS
authors.lastname: Robinson
authors.forename: B L
authors.initials: BL
authors.lastname: Bradley
authors.forename: P K
authors.initials: PK
authors.lastname: Jeffery
authors.forename: S R
authors.initials: SR
authors.lastname: Durham
authors.forename: A B
authors.initials: AB
authors.lastname: Kay
mesh_terms: D000328:Adult; D015703:Antigens, CD / Q000032:analysis; D001249:Asthma / Q000139:chemically induced* / Q000209:etiology; D001706:Biopsy; D001980:Bronchi / Q000473:pathology*; D003485:Cyanates / Q000009:adverse effects*; D004342:Drug Hypersensitivity / Q000209:etiology; D004804:Eosinophils / Q000166:cytology*; D005260:Female; D006649:Histocompatibility Antigens / Q000032:analysis; D006801:Humans; D007150:Immunohistochemistry; D017493:Leukocyte Common Antigens; D008213:Lymphocyte Activation; D008297:Male; D008875:Middle Aged; D009092:Mucous Membrane / Q000098:blood supply / Q000473:pathology; D009784:Occupational Diseases / Q000150:complications; D015375:Receptors, Interleukin-2 / Q000032:analysis; D013601:T-Lymphocytes / Q000276:immunology*
chemical_list: D015703:Antigens, CD; D003485:Cyanates; D006649:Histocompatibility Antigens; D015375:Receptors, Interleukin-2; D017493:Leukocyte Common Antigens