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.
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Authors | L P Schousboe, T Ovesen, C B Pedersen |
Journal | Acta oto-laryngologica. Supplementum
(Acta Otolaryngol Suppl)
Vol. 543
Pg. 89-91
( 2000)
ISSN: 0365-5237 [Print] Norway |
PMID | 10908988
(Publication Type: Journal Article)
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Chemical References |
- Interleukin-1
- Tumor Necrosis Factor-alpha
- Intercellular Adhesion Molecule-1
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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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