Quantitative Analysis of Soluble Cell Adhesion Molecules in Otitis Media with Effusion

Himi, Tetsuo; Kamimura, Masami; Kataura, Akikatsu; Imai, Kohzoh

doi:10.3109/00016489409126057

Cited by 13 publications

(16 citation statements)

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“…However, there have been only a few reports concerning the role of these proteins in the development of otitis media. We previously found significant levels of soluble ICAM-1 in the middle ear effusions of pediatric otitis media [10]. The expression of ICAM-1 in the middle ear mucosa has also been observed in the inflammatory stage of experimentally induced otitis media in rats [11], as well as in other human middle ear effusions [16].…”

Section: Introductionmentioning

confidence: 89%

Expression profile of vascular cell adhesion molecule-1 (CD106) in the middle ear using radiolabeled monoclonal antibody

Himi

Kairemo

Ramsay

1998

European Archives of Oto-Rhino-Laryngology

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Adhesive interactions between leukocytes and endothelium are required for subsequent leukocyte extravasation toward inflammatory sites. Understanding the possible kinetic expression of vascular cell adhesion molecule-1 (VCAM-1) in the middle ear cavity during an inflammatory cascade in vivo may be important for clarifying local immunological responses in otitis media. Two inflammatory models were produced in the rat and involved acute middle ear mucosal and cutaneous inflammation induced after inoculation or intradermal injection of lipopolysaccharide (LPS). After intravenous injection of both 125I-labeled anti-VCAM-1 and 131I-labeled control monoclonal antibody (mAb), the kinetic expression of VCAM-1 in the middle ear and skin was assessed by local radionuclide uptake. The biodistribution of an 125I-labeled anti-VCAM-1 mAb as a potential detector of focal inflammation was examined in normal rats. Both inflammatory lesions were characterized by early and sustained (up to 24 h) expression of VCAM-1, with maximal expression at 4 h after LPS stimulation. The kinetics of VCAM-1 expression was similar among the middle ear mucosa or skin specimens studied and different stimulation methods. A similar biodistribution and clearance of radioactivity between 125I-labeled anti-VCAM-1 mAb and 131I- or 99mTc-labeled control mAb were observed. The present result suggest that functional VCAM-1 induced by LPS is expressed in both middle ear tissue and skin lesions and may play a role in the initial stage of inflammatory response produced. Although VCAM-1 upregulation is a very early event in the inflammatory cascade, 125I-labeled anti-VCAM-1 mAb may be useful for the early detection of focal inflammation in the middle ear.

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Section: Introductionmentioning

confidence: 89%

Expression profile of vascular cell adhesion molecule-1 (CD106) in the middle ear using radiolabeled monoclonal antibody

Himi

Kairemo

Ramsay

1998

European Archives of Oto-Rhino-Laryngology

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“…Limited information on sICAM-1 expression in humans with chronic serous and mucoid otitis media has been previously described. Himi et al (24) measured the levels of sICAM-1 in MEEs of children with chronic serous and mucoid otitis media and found that MEEs contained significantly higher levels of sICAM-1 than the sera of healthy children, but they did not comparatively study serum sICAM-1 levels in children with chronic serous otitis media and children with mucoid otitis media (24). Russo et al studied the ICAM-1 levels in middle ear serous and mucoid effusions in children with otitis media with effusion (a clinical condition distinctly different from AOM) and did not find elevated levels (45).…”

Section: Discussionmentioning

confidence: 99%

Serum Intercellular Adhesion Molecule 1 Variations in Young Children with Acute Otitis Media

Liu

Casey

Pichichero

2010

Clin Vaccine Immunol

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Acute otitis media (AOM) is an inflammatory reaction in the middle ear, most often occurring in young children. Streptococcus pneumoniae, nontypeable Haemophilus influenzae, and Moraxella catarrhalis are the most common bacteria isolated. Intercellular adhesion molecule 1 (ICAM-1) is involved in the innate immune response to infection by microorganisms, in effective antigen presentation, and in subsequent T-cell activation. Here we prospectively studied levels of serum soluble ICAM-1 (sICAM-1) before, at the time of, and after antimicrobial treatment of AOM in a group of 138 children ages 6 to 30 months. Middle ear fluids were collected by tympanocentesis to identify otopathogens. We found that (i) serum levels of sICAM-1 were significantly higher in S. pneumoniae-, nontypeable H. influenzae-, and M. catarrhalis-infected children than in well children (P < 0.001), confirming that a systemic inflammatory response occurs during AOM; (ii) sICAM-1 levels varied from no elevation (110 ng/ml) to elevation to high levels (maximum, 1,470 ng/ml) among children with AOM; (iii) in paired samples, sICAM-1 levels increased 4-to 20-fold when children developed AOM compared to their sICAM-1 levels before infection; and (iv) the level of sICAM-1 returned to the pre-AOM level at the convalescent stage of AOM after successful antimicrobial therapy. We conclude that AOM often causes a systemic inflammatory reaction, as measured by elevation of the serum sICAM-1 level, and that a high variability in sICAM-1 responses occurs with the presence of otopathogens during AOM.Acute otitis media (AOM) is defined by the presence of middle ear effusion (MEE) with acute onset of symptoms of inflammation of the middle ear. Although more than half of patients who develop AOM have fever (14), the condition is considered a localized, mucosal infection. Currently, AOM is regarded as relatively benign due to spontaneous resolution of the infection in a majority of patients (42). The complications and sequelae of bacterial systemic invasion from the middle ear, including mastoiditis, brain abscess, and meningitis, are sufficiently rare that they have recently been considered less consequential in comparison to the consequences from the costs of antimicrobial treatment and overtreatment (2).The cause and pathogenesis of otitis media are multifactorial, involving viral and bacterial infections. The most frequently isolated bacteria in AOM are Streptococcus pneumoniae (20 to 55% of cases), nontypeable Haemophilus influenzae (15 to 40%), and Moraxella catarrhalis (10 to 25%) (12,25,29). When bacteria gain entry into the middle ear space, they damage the middle ear mucosa directly by releasing toxins and indirectly by provoking both specific immunological and general inflammatory responses in the host. A prominent feature of the host response is an influx of inflammatory cells into the middle ear.The migration of leukocytes into sites of inflammation is mediated by numerous factors, including intercellular adhesion molecule 1 (ICAM-1; CD54). ICAM-1 is a m...

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“…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.…”

Section: T Cells Activated Cd8mentioning

confidence: 99%

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

Lim¹,

Hyun²,

Kim³

et al. 2018

Korean J Otorhinolaryngol-Head Neck Surg

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Inflammation in the middle ear mucosa, which can be provoked by different primary factors such as bacterial and viral infection, local allergic reactions and reflux, is the crucial event in the pathogenesis of otitis media with effusion (OME). Unresolved acute inflammatory responses or defective immunoregulation of middle inflammation can promote chronic inflammatory processes and stimulate the chronic condition of OME. Cytokines are the central molecular regulators of middle ear inflammation and can switch the acute phase of inflammation in the chronic stage and induce molecular Á /pathological processes leading to the histopathological changes accompanying OME. In this review we present cytokines identified in otitis media, immunoregulatory [interleukin (IL)-2, IL-10, transforming growth factorb]) and allergy associated (IL-4, IL-5, granulocyte Á / macrophage colony-stimulating factor), as crucial molecular regulators, responsible for chronic inflammation in the middle ear and the chronic condition of OME.

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Quantitative Analysis of Soluble Cell Adhesion Molecules in Otitis Media with Effusion

Cited by 13 publications

References 16 publications

Expression profile of vascular cell adhesion molecule-1 (CD106) in the middle ear using radiolabeled monoclonal antibody

Expression profile of vascular cell adhesion molecule-1 (CD106) in the middle ear using radiolabeled monoclonal antibody

Serum Intercellular Adhesion Molecule 1 Variations in Young Children with Acute Otitis Media

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

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