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 Arch Allergy Immunol. 1999 Jun;119(2):120-5. doi: 10.1159/000024186.


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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Asthma / genetics
  • Asthma / pathology*
  • Biopsy
  • Bronchi / metabolism*
  • Bronchi / pathology
  • Female
  • Humans
  • Hypersensitivity, Immediate / pathology
  • Interleukin-16 / genetics
  • Interleukin-16 / immunology
  • Interleukin-16 / metabolism*
  • Male
  • Mucous Membrane / metabolism
  • Phenotype


  • Interleukin-16