In vitro study of IL-8 and goblet cells: possible role of IL-8 in the aetiology of otitis media with effusion

Acta Otolaryngol. 2002 Mar;122(2):146-52. doi: 10.1080/00016480252814144.


One of the main characteristics of otitis media with effusion (OME) is the differentiation of basal cells into goblet cells with subsequent proliferation in a modified respiratory epithelium leading to the formation of mucin-rich effusion in the middle ear cleft. In order to determine the effect of pro-inflammatory cytokines identified in OME, e.g. IL-1beta, tumour necrosis factor (TNF)-alpha, IL-6 and IL-8, on goblet cells, and to clarify the role of IL-8 in particular, we used the human goblet cell line HT29-MTX, which secretes two OME-related mucins: MUC5AC and MUC5B. IL-1beta and TNF-alpha stimulated the secretion of IL-8 in HT29-MTX goblet cells. Dose- (2-200 ng/ml) and time- (0-5 days) response studies of IL-8-induced mucin secretion were carried out. IL-8 upregulated the secretion of MUC5AC and MUC5B mucins in a concentration-dependent manner, with a maximum response at an IL-8 concentration of 20 ng/ml. IL-8 (20 ng/ml)-mediated mucin secretion persisted for up to 5 days, with a peak response 72 h after the addition of cytokine. These results suggest that: (i) goblet cells are target cells for the pro-inflammatory cytokines IL-1beta, TNF-alpha and IL-8 and can contribute to the pathogenesis of OME by increasing both the concentration of IL-8 and the secretion of mucin; and (ii) IL-8 stimulates prolonged mucin secretion from goblet cells and may be involved in the maintenance of the disease in the chronic stage.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Differentiation
  • Cytokines / pharmacology
  • Cytokines / physiology
  • Ear, Middle / cytology
  • Goblet Cells / cytology
  • Goblet Cells / metabolism*
  • HT29 Cells
  • Humans
  • Inflammation Mediators / pharmacology
  • Inflammation Mediators / physiology
  • Interleukin-8 / metabolism*
  • Mucins / metabolism
  • Otitis Media with Effusion / etiology*


  • Cytokines
  • Inflammation Mediators
  • Interleukin-8
  • Mucins