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
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.