Phenotype of IL-16-producing cells in bronchial mucosa: Evidence for the human eosinophil and mast cell as cellular sources of IL-16 in asthma

Citation
S. Laberge et al., Phenotype of IL-16-producing cells in bronchial mucosa: Evidence for the human eosinophil and mast cell as cellular sources of IL-16 in asthma, INT A AL IM, 119(2), 1999, pp. 120-125
Citations number
27
Categorie Soggetti
Immunology
Journal title
INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY
ISSN journal
10182438 → ACNP
Volume
119
Issue
2
Year of publication
1999
Pages
120 - 125
Database
ISI
SICI code
1018-2438(199906)119:2<120:POICIB>2.0.ZU;2-U
Abstract
Background: We have previously shown increased expression of the CD4+ cell chemoattractant interleukin (IL)-16 in bronchial biopsies of atopic asthmat ic subjects compared to normal controls. IL-16 immunoreactive cells were id entified as both epithelial cells and nonepithelial inflammatory cells. The aim of this study was to characterize and compare the phenotype of non-epi thelial inflammatory cells that express IL-16 immunoreactivity in bronchial biopsies from non-atopic normal controls and atopic asthmatic subjects. Me thods: Sections from endobronchial biopsies obtained from nonatopic normal controls and atopic asthmatics were processed for double immunocytochemistr y. IL-16 immunoreactivity was assessed using a polyclonal anti-IL-16 antibo dy and the avidin-biotin complex-diaminobenzidine method. The phenotype of IL-16 immunoreactive cells was assessed using anti-CD3, anti-MBP, anti-tryp tase and anti-CD68 mAbs and the alkaline phosphatase complex-fast Red metho d. Results: In normal subjects, the majority of IL-16 immunoreactive cells were CD3+ T cells (71.1+/-10.3%) and CD68+ macrophages (22.4+/-8.1%). IL-16 immunoreactivity coexpressed with tryptase+ mast cells in 4 of 7 normal su bjects whereas IL-16 immunoreactivity coexpressed with MBP+ eosinophils in only 1 normal subject. In atopic asthmatic subjects, IL-16 immunoreactive c ells were mainly CD3+ T cells (60.8+/-8.7%) and MPB+ eosinophils (16.8+/-8. 2%). IL-16 immunoreactivity also coexpressed with tryptase+ mast cells (10. 6+/-4.0%) in all asthmatic subjects. The number of IL-16 immunoreactive cel ls that coexpressed MBP was higher in asthmatic subjects compared to normal controls (p=0.003). Conclusion: Our data show that T cells are the major n on-epithelial cellular source of IL-16 in normal and asthmatic airways, Eos inophils and mast cells comprised other potential cellular sources of IL-16 in asthmatic airways.