Endotoxin, tumour necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL
-IP) and intercellular adhesion molecule-1 (ICAM-1) were detected in 88%, 5
1%, 58% and 66% of 152 middle ears from patients suffering from otitis medi
a 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 ep
ithelium 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 imm
unosorbent assay on the cell layer. For TNF-alpha, 5 ng/ml significantly in
creased ICAM-1 expression, whereas 100 ng/ml had a toxic effect, For IL-1 b
eta, as little as 1 ng/ml produced a significant increase in ICAM-1 express
ion. Endotoxin stimulated ICAM-1 expression less strongly in concentrations
from 100 ng/ml to 100 mu g/ml. The findings indicate that stimulation of I
CAM-1 by endotoxin is mediated, at least in part, by TNF-alpha and IL-1 bet
a. It is concluded that endotoxin induces sustained inflammation in OME, an
d that this inflammation is mediated, at least in part, by the primary cyto
kines TNF-alpha and IL-1 beta.