Inflammatory Mediators in Chronic Otitis Media With Effusion

Abstract

\s=b\Otitis media with effusion (OME) is a common middle ear inflammatory disease in the pediatric population. This article determines concentrations of three functionally and metabolically distinct inflammatory mediators in middle ear effusions (MEE) and corresponding plasma of children with OME. One hundred two patients (mean age, 4.9 years) with persistent OME were studied. Middle ear effusions were collected from all subjects and plasma from a subset at the time of tympanostomy tube insertion. Histamine was assayed radioisotopically, 13, 14-dihydro-15-keto-prostaglandin F2\g=a\(stable PGF2\g=a\ metabolite) by radioimmunoassay, and neutrophil chemotactic factor of anaphylaxis by modified Boyden chamber. Mean MEE levels of the mediators (39 \m=+-\ 13 ng/mL, 462 \m=+-\179 pg/mL, and 264% \ m=+-\ 57% positive control, respectively) were markedly higher than those of corresponding plasma (0.5 \m=+-\ 0.1 ng/mL, 285 \m=+-\127 pg/mL, and 47% \m=+-\5% positive control, respectively). The mean histamine content of mucoid effusions (43.2 \ m=+-\56.9 ng/mL) was significantly higher than that of purulent (22.5 \m=+-\10.5 ng/mL) and serous (17.9 \m=+-\ 16.8 ng/mL) effusions. Higher histamine levels were observed in effusions positive for Haemophilus influenzae when compared with those with other pathogenic isolates. The high concentrations of these mediators in MEE and their potential for inducing or sustaining the inflammatory process supports a role in the pathogenesis of OME. (Arch Otolaryngol Head Neck Surg 1988;114:1131-1133 Otitis media with effusion (OME) is a middle ear inflammatory dis¬ ease that is common in the pediatrie population. A variety of potent inflammatory mediators has been detected in middle ear effusions (MEE) of children with OME.1 More¬ over, a role for these mediators in the pathogenesis and maintenance of the disease condition was emphasized by the results of a number of recent experimental studies using animal models.2 In humans, IgE-dependent mediator release or allergy has also been incriminated as a risk factor in OME. This investigation determined MEE concentrations of two mast cellderived mediators, histamine and neutrophil chemotactic factor of anaphylaxis (NCF-A), and a stable metabolite of prostaglandin (PG)F2o. The latter two have not been previous¬ ly studied in OME. PATIENTS AND METHODSOne hundred two patients, aged 1 to 23 years (mean age, 4.9 years) with docu¬ mented persistent OME unresponsive to antimicrobial therapy were enrolled after obtaining informed consent. All patients had tympanostomy tubes inserted at which time MEEs were collected. Unilateral effu¬ sions were collected from 25 patients and bilateral effusions were collected from the remaining 17 patients. These samples were classified visually as serous, mucoid, or purulent; cultured immediately for aerobic bacteria; and a subset was submitted for complete cell count by Coulter Counter and differential. The remaining fluid (50 to 200

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

“…In addition, middle ear mast cells were increased twofold in patients with chronic middle ear disease (129). Histamine levels were found to be higher in mucoid effusions than serous-type effusions (121, 129). Thus, histamine appears to be an important mediator influencing both acute and chronic OME.…”

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.…”

The Relation between Tympanostomy Tube Otorrhea and Types of Immune Cells in Middle Ear Effusion in Children with Otitis Media with Effusion

“…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.…”