Middle ear epithelium has inflammatory capacity.
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.
Schousboe
L P
LP
Department of Otorhinolaryngology, Aarhus University Hospital, Denmark.
Ovesen
T
T
Pedersen
C B
CB
D000818:Animals; D004432:Ear, Middle / Q000378:metabolism*; D004847:Epithelial Cells / Q000378:metabolism; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D007375:Interleukin-1 / Q000378:metabolism; D010034:Otitis Media with Effusion / Q000378:metabolism*; D011817:Rabbits; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D007375:Interleukin-1; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1