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Middle ear epithelium has inflammatory capacity.

Abstract
Endotoxin, tumour necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta) and intercellular adhesion molecule-1 (ICAM-1) were detected in 88%, 51%, 58% and 66% of 152 middle ears from patients suffering from otitis media with effusion. In this study the hypothesis that bacterial endotoxin, TNF-alpha, IL-1 beta and ICAM-1 induce the inflammatory process characteristic of otitis media with effusion was tested. Cultures of rabbit middle ear epithelium were exposed to endotoxin, TNF-alpha or IL-1 beta. The expression of ICAM-1 on the cell surfaces was measured with a direct enzyme-linked immunosorbent assay on the cell layer. For TNF-alpha, 5 ng/ml significantly increased ICAM-1 expression, whereas 100 ng/ml had a toxic effect. For IL-1 beta, as little as 1 ng/ml produced a significant increase in ICAM-1 expression. Endotoxin stimulated ICAM-1 expression less strongly in concentrations from 100 ng/ml to 100 micrograms/ml. The findings indicate that stimulation of ICAM-1 by endotoxin is mediated, at least in part, by TNF-alpha and IL-1 beta. It is concluded that endotoxin induces sustained inflammation in OME, and that this inflammation is mediated, at least in part, by the primary cytokines TNF-alpha and IL-1 beta.
AuthorsL P Schousboe, T Ovesen, C B Pedersen
JournalActa oto-laryngologica. Supplementum (Acta Otolaryngol Suppl) Vol. 543 Pg. 89-91 ( 2000) ISSN: 0365-5237 [Print] Norway
PMID10908988 (Publication Type: Journal Article)
Chemical References
  • Interleukin-1
  • Tumor Necrosis Factor-alpha
  • Intercellular Adhesion Molecule-1
Topics
  • Animals
  • Ear, Middle (metabolism)
  • Epithelial Cells (metabolism)
  • Intercellular Adhesion Molecule-1 (metabolism)
  • Interleukin-1 (metabolism)
  • Otitis Media with Effusion (metabolism)
  • Rabbits
  • Tumor Necrosis Factor-alpha (metabolism)

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