How does endotoxin trigger inflammation in otitis media with effusion?

Citation
Lp. Schousboe et al., How does endotoxin trigger inflammation in otitis media with effusion?, LARYNGOSCOP, 111(2), 2001, pp. 297-300
Citations number
15
Categorie Soggetti
Otolaryngology
Journal title
LARYNGOSCOPE
ISSN journal
0023852X → ACNP
Volume
111
Issue
2
Year of publication
2001
Pages
297 - 300
Database
ISI
SICI code
0023-852X(200102)111:2<297:HDETII>2.0.ZU;2-N
Abstract
Objectives: The relationship among microorganisms, endotoxin, and inflammat ory mediators in otitis media with effusion (OME) was examined. Study Desig n: Analysis of 152 middle ear effusions aspirated at the time of ventilatio n tube insertion from children with OME. Methods: Effusion samples were cul tured for pathogenic bacteria. The two primary cytokines, interleukin-1 bet a (IL1 beta) and tumor necrosis factor (TNF alpha), and the adhesion molecu les, intercellular and vascular adhesion molecule (ICAM-1 and VCAM-1), were quantified using the enzyme-linked immunosorbent assay (ELISA) technique. Endotoxin concentration was measured with a limulus amebocyte lysate assay, and total protein concentration was quantified using the Biorad microassay , Results: The cultures of pathogenic bacteria were positive in 33 of the 1 52 effusions (22%), which contained more endotoxin and more of the primary cytokines than the 119 culture-negative effusions, Endotoxin and the primar y cytokines were positively correlated, both in the whole material and in t he sterile effusions alone. The adhesion molecules were positively correlat ed with each other, but not with endotoxin or the primary cytokines. Conclu sions: We found a positive correlation between endotoxin and the primary cy tokines TNF alpha and IL1 beta in culture-positive OME effusions as well as in culture-negative ones, suggesting endotoxin-induced local production of TNF alpha and IL1 beta in the middle ear. ICAM-1 and VCAM-1 were also pres ent in the middle ear, but their concentrations were not directly correlate d to endotoxin or the primary cytokines.