title: Phenotype of cells expressing mRNA for TH2-type (interleukin 4 and interleukin 5) and TH1-type (interleukin 2 and interferon gamma) cytokines in bronchoalveolar lavage and bronchial biopsies from atopic asthmatic and normal control subjects.
abstract: We investigated the phenotype of cells expressing messenger RNA encoding interleukin 4 (IL-4), IL-5, IL-2, and interferon gamma (IFN-gamma) in bronchoalveolar lavage (BAL) and bronchial biopsies (BX) from seven mild atopic asthmatic patients and nine nonasthmatic controls. Immunocytochemistry followed by in situ hybridization using either 35S- or digoxigenin-labeled riboprobes was performed on cytospins from BAL and BX, respectively. With BAL or BX, in situ hybridization alone showed significant increases in percentages of IL-2, IL-4, and IL-5 mRNA+ cells when asthmatics were compared to nonasthmatic controls. Double immunocytochemistry-in situ hybridization revealed that > 70% of IL-4 and IL-5 mRNA+ cells were activated T cells (CD3+). The remaining IL-4 and IL-5 mRNA+ signals were colocalized to tryptase+ mast cells, and activated eosinophils (EG2+). Rare IL-4 and IL-5 mRNA+ cells were observed in nonasthmatic controls, the majority being CD3+ cells, as were IL-2 and IFN-gamma mRNA+ cells (in both asthmatics and controls). A few IL-4 (< 8%) and IL-5 (< 5%) mRNA+ signals did not colocalize with any of the cells identified by immunocytochemistry. Thus, we provide further evidence that CD3+ T cells are the most abundant cells expressing IL-4 and IL-5 mRNA in BAL and BX from allergic asthma. Fewer, but detectable, numbers of tryptase+ mast cells and EG2+ eosinophils also expressed these transcripts.
authors.affiliation: Department of Allergy and Clinical Immunology, National Heart and Lung Institute, London, United Kingdom.
authors.forename: S
authors.initials: S
authors.lastname: Ying
authors.forename: S R
authors.initials: SR
authors.lastname: Durham
authors.forename: C J
authors.initials: CJ
authors.lastname: Corrigan
authors.forename: Q
authors.initials: Q
authors.lastname: Hamid
authors.forename: A B
authors.initials: AB
authors.lastname: Kay
mesh_terms: D000328:Adult; D015703:Antigens, CD / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism; D001249:Asthma / Q000276:immunology*; D001980:Bronchi / Q000166:cytology / Q000378:metabolism; D001992:Bronchoalveolar Lavage Fluid; D017252:CD3 Complex / Q000378:metabolism; D053818:Chymases; D004804:Eosinophils / Q000378:metabolism; D005260:Female; D006801:Humans; D006967:Hypersensitivity / Q000276:immunology*; D007371:Interferon-gamma / Q000235:genetics / Q000378:metabolism*; D007376:Interleukin-2 / Q000235:genetics / Q000378:metabolism*; D015847:Interleukin-4 / Q000235:genetics / Q000378:metabolism*; D015848:Interleukin-5 / Q000235:genetics / Q000378:metabolism*; D008297:Male; D012697:Serine Endopeptidases / Q000378:metabolism; D018417:Th1 Cells / Q000378:metabolism*; D018418:Th2 Cells / Q000378:metabolism*; D053802:Tryptases; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D017252:CD3 Complex; D053818:Chymases; D007371:Interferon-gamma; D007376:Interleukin-2; D015847:Interleukin-4; D015848:Interleukin-5; D012697:Serine Endopeptidases; D053802:Tryptases; C067980:CD68 antigen, human; D000097382:CD68 Molecule; C083294:chymase 2