title: Increased interleukin-10 messenger RNA expression in atopic allergy and asthma.
abstract: Interleukin-10 (IL-10) inhibits T-lymphocyte proliferation and production of cytokines. We have examined expression of IL-10 messenger RNA (mRNA) in atopic asthma and in allergen and tuberculin skin responses by in situ hybridization. The proportion of bronchoalveolar lavage (BAL) cells positive for IL-10 mRNA was increased in a group of 10 symptomatic asthmatics when compared with control subjects (17.5% versus 5.2% BAL cells positive; P < 0.001). In a separate group of six mild atopic asthmatics, there was an increased proportion of BAL cells positive for IL-10 mRNA 24 h after allergen inhalation challenge compared with diluent challenge BAL from the same subjects (24% versus 10%; P < 0.005). By simultaneous in situ hybridization and immunocytochemistry, IL-10 mRNA was localized to both CD3+ T cells and CD68+ alveolar macrophages in BAL, with a significantly more prominent T-cell signal in the symptomatic asthmatics compared with control subjects and after allergen challenge compared with diluent challenge of the mild asthmatic subjects. It has been suggested that IL-10 production is a late event after T-cell activation. To examine kinetics and specificity of IL-10 mRNA expression, skin biopsies were obtained from atopic, tuberculin-sensitive subjects at 1, 6, and 48 h after cutaneous injection of allergen or tuberculin. With both stimuli, there was an increase in IL-10 mRNA-positive cells at 6 h when compared with control sites injected with appropriate diluent which were biopsied 24 h after injection (P < 0.01 for allergen and P < 0.02 for tuberculin). These findings are compatible with the hypothesis that IL-10 mRNA is expressed in both macrophages and T lymphocytes in the airway in asthma and that IL-10 mRNA expression is induced from T lymphocytes in response to allergen. This response may also occur in other types of cell-mediated inflammation.
authors.affiliation: National Heart and Lung Institute, London, United Kingdom.
authors.forename: D S
authors.initials: DS
authors.lastname: Robinson
authors.forename: A
authors.initials: A
authors.lastname: Tsicopoulos
authors.forename: Q
authors.initials: Q
authors.lastname: Meng
authors.forename: S
authors.initials: S
authors.lastname: Durham
authors.forename: A B
authors.initials: AB
authors.lastname: Kay
authors.forename: Q
authors.initials: Q
authors.lastname: Hamid
mesh_terms: D000293:Adolescent; D000328:Adult; D000485:Allergens / Q000494:pharmacology; D000704:Analysis of Variance; D001249:Asthma / Q000235:genetics* / Q000276:immunology; D001706:Biopsy; D018893:Bronchoalveolar Lavage; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry / Q000166:cytology; D005260:Female; D015870:Gene Expression / Q000276:immunology; D006801:Humans; D006968:Hypersensitivity, Delayed / Q000235:genetics / Q000276:immunology; D006969:Hypersensitivity, Immediate / Q000235:genetics* / Q000276:immunology; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D016753:Interleukin-10 / Q000235:genetics* / Q000276:immunology; D008297:Male; D008875:Middle Aged; D012333:RNA, Messenger / Q000235:genetics; D012680:Sensitivity and Specificity; D012867:Skin / Q000166:cytology / Q000276:immunology
chemical_list: D000485:Allergens; D012333:RNA, Messenger; D016753:Interleukin-10