BACKGROUND: We have previously shown increased expression of the CD4+ cell chemoattractant interleukin (IL)-16 in bronchial biopsies of atopic asthmatic subjects compared to normal controls. IL-16 immunoreactive cells were identified as both epithelial cells and non-epithelial inflammatory cells. The aim of this study was to characterize and compare the phenotype of non-epithelial inflammatory cells that express IL-16 immunoreactivity in bronchial biopsies from non-atopic normal controls and atopic asthmatic subjects. METHODS: Sections from endobronchial biopsies obtained from non-atopic normal controls and atopic asthmatics were processed for double immunocytochemistry. IL-16 immunoreactivity was assessed using a polyclonal anti-IL-16 antibody and the avidin-biotin complex-diaminobenzidine method. The phenotype of IL-16 immunoreactive cells was assessed using anti-CD3, anti-MBP, anti-tryptase and anti-CD68 mAbs and the alkaline phosphatase complex-Fast Red method. 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 subjects whereas IL-16 immunoreactivity coexpressed with MBP+ eosinophils in only 1 normal subject. In atopic asthmatic subjects, IL-16 immunoreactive cells 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 cells 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 non-epithelial cellular source of IL-16 in normal and asthmatic airways. Eosinophils and mast cells comprised other potential cellular sources of IL-16 in asthmatic airways.
BACKGROUND: We have previously shown increased expression of the CD4+ cell chemoattractant interleukin (IL)-16 in bronchial biopsies of atopic asthmatic subjects compared to normal controls. IL-16 immunoreactive cells were identified as both epithelial cells and non-epithelial inflammatory cells. The aim of this study was to characterize and compare the phenotype of non-epithelial inflammatory cells that express IL-16 immunoreactivity in bronchial biopsies from non-atopic normal controls and atopic asthmatic subjects. METHODS: Sections from endobronchial biopsies obtained from non-atopic normal controls and atopic asthmatics were processed for double immunocytochemistry. IL-16 immunoreactivity was assessed using a polyclonal anti-IL-16 antibody and the avidin-biotin complex-diaminobenzidine method. The phenotype of IL-16 immunoreactive cells was assessed using anti-CD3, anti-MBP, anti-tryptase and anti-CD68 mAbs and the alkaline phosphatase complex-Fast Red method. 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 subjects whereas IL-16 immunoreactivity coexpressed with MBP+ eosinophils in only 1 normal subject. In atopic asthmatic subjects, IL-16 immunoreactive cells 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 cells 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 non-epithelial cellular source of IL-16 in normal and asthmatic airways. Eosinophils and mast cells comprised other potential cellular sources of IL-16 in asthmatic airways.
Authors: Nguyen Phuong Khanh Le; Amanda Florentina do Nascimento; David Schneberger; Chi Cuong Quach; Xiaobei Zhang; Gurpreet K Aulakh; Wojciech Dawicki; Lixin Liu; John R Gordon; Baljit Singh Journal: Respir Res Date: 2022-06-22