Increased expression of interleukin-16 in bronchial mucosa of subjects with atopic asthma

Am J Respir Cell Mol Biol. 1997 Aug;17(2):193-202. doi: 10.1165/ajrcmb.17.2.2750.


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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Asthma / metabolism*
  • Asthma / pathology
  • Biopsy
  • Bronchi / metabolism*
  • Bronchi / pathology
  • Bronchoscopy
  • CD4-Positive T-Lymphocytes / cytology
  • Female
  • Humans
  • Interleukin-16 / genetics*
  • Male
  • Mucous Membrane / metabolism
  • Mucous Membrane / pathology
  • RNA, Messenger / genetics


  • Interleukin-16
  • RNA, Messenger