Soluble adhesion molecules in middle ear effusions from patients with chronic otitis media with effusion

Abstract

Soluble forms of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) have been identified in the peripheral blood and other body fluids. These soluble adhesion molecules have been reported to reflect the upregulation of cell surface ICAM-1 and VCAM-1 expression in inflammatory diseases. The levels of soluble ICAM-1 and soluble VCAM-1 in 37 middle ear effusions from 37 patients with chronic otitis media with effusion (OME) were quantitatively determined with enzyme-linked immunosorbent assays. The levels of soluble ICAM-1 in mucoid effusions were significantly higher than those in serous effusions, but the levels of soluble VCAM-1 did not differ significantly between the two types of effusion. The levels of soluble VCAM-1 in effusions from atopic patients were significantly higher than those from non-atopic patients, whereas the levels of soluble ICAM-1 in samples from atopic patients were significantly lower than those from non-atopic patients. Therefore, our data suggest that an increase in soluble VCAM-1 plays a more important role in the pathogenesis of OME in atopic patients than in non-atopic patients. In addition, soluble ICAM-1 is likely to play a more important role in the pathogenesis of OME in nonatopic patients than soluble VCAM-1.

The Role of Inflammatory Mediators in the Pathogenesis of Otitis Media and Sequelae

“…PAF also stimulates secretion of mucus glycoprotein mediated by arachidonic acid metabolites, especially metabolites of the lipoxygenase pathway via a PAF-receptor dependent mechanism (244), and inhibits mucociliary clearance of the eustachian tube (245). The expression of soluble adhesion molecules, such as intercellular adhesion molecule-1 (ICAM-1), is known to be upregulated at the cell surface in inflammatory disease.…”

The immunoregulatory and allergy‐associated cytokines in the aetiology of the otitis media with effusion

“…Different groups of inflammatory mediators were identified in the human middle ear mucosa, fluids and effusions. A lot of different mediators participate in initiation and early stages of the middle ear inflammation, including arachidonic acid metabolites (prostaglandin E 2 and leukotrienes LT-B 4 , LT-C 4 ), 75,76 histamine, 77,78 platelet-activating factor, 79 surface cell adhesion molecules (intercellular adhesion molecule-1, vascular cell adhesion molecule-1, endothelial leukocyte adhesion molecule-1, platelet endothelial cell adhesion molecule), 80,81 soluble cell adhesion molecules (soluble intercellular adhesion molecule-1 and soluble vascular cell adhesion molecule-1), 82,83 chemokine RANTES, 84 complement C3a anaphylatoxin 85 and interferon-g. 86 However, cytokines are the key mediators of the middle ear inflammation. Cytokines regulate different stages of inflammation, are responsible for resolution of inflammation and can initiate local molecular processes leading to histopathological changes in the middle ear mucosa and submucosa, and the chronic condition of otitis media.…”

How Does Endotoxin Trigger Inflammation in Otitis Media With Effusion?

“…The present results are comparable to previous reports. 4–7,9,13 To our knowledge, we present the largest OME study group described. In accordance with our study, a high correlation among endotoxin, TNFα, and IL1β was recently reported in a similar patient group.…”

“… 6 There is only one previous report of adhesion molecules in middle ear effusions describing a correlation between ICAM‐1 and VCAM‐1 like in our findings. 13 The variation in concentration ranges between studies could be the result of different inclusion criteria along with features of the measuring methods, including sensitivity and detection percentage. We wanted to include chronic OME cases, excluding AOM and recurrent AOM cases.…”