Increased Expression of Interleukin-16 in Bronchial Mucosa of Subjects with Atopic Asthma
- 1 August 1997
- journal article
- Published by American Thoracic Society in American Journal of Respiratory Cell and Molecular Biology
- Vol. 17 (2), 193-202
- https://doi.org/10.1165/ajrcmb.17.2.2750
Abstract
Asthma is characterized by the presence of activated CD4+ cells in the airways. We hypothesized that the newly characterized cytokine interleukin (IL)-16 is involved in the pathogenesis of asthma through its ability to selectively induce CD4+ cell recruitment within the inflamed bronchial wall. We investigated the expression of IL-16 in bronchial biopsies obtained from subjects with mild asthma (n = 10), atopic nonasthmatic individuals (n = 6), and normal control subjects (n = 10). Cryostat sections from 4% paraformaldehyde-fixed fiberoptic bronchial biopsies were immunostained using a specific antibody that recognizes human IL-16. IL-16 mRNA expression was determined by in situ hybridization. IL-16 immunoreactivity and mRNA were demonstrated mainly in bronchial epithelial cells in all subjects. IL-16 immunoreactivity and IL-16 mRNA expression within the epithelium were significantly higher in bronchial biopsies obtained from asthmatic subjects as compared to both atopic nonasthmatic and normal controls (P < 0.001). The numbers of subepithelial IL-16 immunoreactive cells and IL-16 mRNA-positive cells were also greater in the bronchial biopsies obtained from asthmatic subjects as compared to both atopic nonasthmatic and normal controls (P < 0.001). Epithelial expression of IL-16 immunoreactivity and mRNA correlated with the CD4+ cell infiltration (r2 = 0.70, P < 0.001). There were significant associations between epithelial and subepithelial IL-16 immunoreactivity and airway responsiveness to methacholine. This study demonstates that IL-16 is expressed in airway tissues, particularly in the epithelial cells, and that up-regulation of its expression is a feature of allergic asthma. These results suggest an in vivo role for IL-16 in the pathogenesis of asthma, possibly through the recruitment of CD4+ cells, and support the increasing evidence for the participation of epithelial cells in regulating inflammatory responses.Keywords
This publication has 40 references indexed in Scilit:
- Airway Mucosal Inflammation Even in Patients with Newly Diagnosed AsthmaAmerican Review of Respiratory Disease, 1993
- Eosinophils express interleukin 5 and granulocyte macrophage-colony-stimulating factor mRNA at sites of allergic inflammation in asthmatics.JCI Insight, 1992
- Lymphocyte Activation in Bronchoalveolar Lavage and Peripheral Blood in Atopic AsthmaAmerican Review of Respiratory Disease, 1992
- Eosinophils, T-lymphocytes, mast cells, neutrophils, and macrophages in bronchial biopsy specimens from atopic subjects with asthma: Comparison with biopsy specimens from atopic subjects without asthma and normal control subjects and relationship to bronchial hyperresponsivenessJournal of Allergy and Clinical Immunology, 1991
- Expression of mRNA and immunoreactivity for the granulocyte/macrophage colony-stimulating factor in activated human eosinophils.The Journal of Experimental Medicine, 1991
- Dynamic T-Cell Changes in Peripheral Blood and Bronchoalveolar Lavage after Antigen Bronchoprovocation in AsthmaticsAmerican Review of Respiratory Disease, 1991
- Identification of Activated T Lymphocytes and Eosinophils in Bronchial Biopsies in Stable Atopic AsthmaAmerican Review of Respiratory Disease, 1990
- Mucosal Inflammation in AsthmaAmerican Review of Respiratory Disease, 1990
- The eosinophil and bronchial asthma: Current understandingJournal of Allergy and Clinical Immunology, 1990
- Cellular Events in the Bronchi in Mild Asthma and after Bronchial ProvocationAmerican Review of Respiratory Disease, 1989