Neutrophil Oxygen Metabolite Inhibition of Cultured Chinchilla Middle Ear Epithelial Cell Growth

Kawana, Masahiro; Kawana, C; Juhn, Steven K.; Amesara, Ryo; Giebink, G. Scott

doi:10.1177/000348949410301012

Cited by 3 publications

(1 citation statement)

References 23 publications

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“…Neutrophils release free radicals such as H202, which may inhibit the cell nietabolism and thus prolong the niiddle ear inflammatory response and lead to chronic tissue damage. The effect of neutrophil metabolic products on middle ear epithelial cells of the chinchilla was studied in vitro by Kawana et al [20]. They demonstrated that cell growth was inhibited by activated neutrophils whereas tinstimulated neutrophils did not affect the viability of these cells.…”

Section: Effusionmentioning

confidence: 99%

New views on the pathogenesis of acute otitis media and its complications

François

1997

Clinical Microbiology and Infection

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The pathogenesis of acute otitis media is complex and multifactorial. Bacteria infecting the middle ear come from the nasopharynx via the eustachian tube. This colonization is facilitated by bacterial adherence on the pharyngeal and the eustachian tube cells. Otitis media is characterized by inflammation of the middle ear with an infiltration of the subperiosteal space by leukocytes, macrophages and mast cells. The effusion contains great amounts of inflammatory mediators (eicosanoids, cytokines, histamine). Elimination of the effusion and/or the bacteria is based on non-specific factors such as mucociliary clearance and phagocytosis, and on a specific immune response which apparently is not the same for Haemophilus influenzae and for Streptococcus pneumoniae. The main complications of acute otitis media are otitis media with effusion, mastoiditis, sensorineural hearing loss and meningitis.

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Section: Effusionmentioning

confidence: 99%

New views on the pathogenesis of acute otitis media and its complications

François

1997

Clinical Microbiology and Infection

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Early Inflammatory Changes of the Haemophilus influenzae-Induced Experimental Otitis Media

Kawana

1995

Auris Nasus Larynx

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Otitis Media: The Chinchilla Model1

1999

Microbial Drug Resistance

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Streptococcus pneumoniae infection and disease have been modeled in several animal species including infant and adult mice, infant and adult rats, infant Rhesus monkeys, and adolescent and adult chinchillas. Most are models of sepsis arising from intravenous or intraperitoneal inoculation of bacteria, and a few were designed to study disease arising from intranasal infection. Chinchillas provide the only animal model of middle ear pneumococcal infection in which the disease can be produced by very small inocula injected into the middle ear (ME) or intranasally, and in which the disease remains localized to the ME in most cases. This model, developed at the University of Minnesota in 1975, has been used to study pneumococcal pathogenesis at a mucosal site, immunogenicity and efficacy of pneumococcal capsular polysaccharide (PS) vaccine antigens, and the kinetics and efficacy of antimicrobial drugs. Pathogenesis experiments in the chinchilla model have revealed variation in ME virulence among different pneumococcal serotypes, enhancement of ME infection during concurrent intranasal influenza A virus infections, and natural resolution of pneumococcal otitis media (OM) without intervention. Research has explored the relative contribution of pneumococcal and host products to ME inflammation. Pneumococcal cell wall components and pneumolysin have been studied in the model. Host inflammatory responses studied in the chinchilla ME include polymorphonuclear leukocyte oxidative products, hydrolytic enzymes, cytokine and eicosanoid metabolites, and ME epithelial cell adhesion and mucous glycoprotein production. Both clinical (tympanic membrane appearance) and histopathology (ME, Eustachian tube, inner ear) endpoints can be quantified. Immunologic and inflammatory studies have been facilitated by the production of affinity-purified antichinchilla immunoglobulin G (IgG), IgM, and secretory IgA polyclonal antibody reagents, and the identification of cross-reactivity between human and chinchilla cytokines, and between guinea pig and chinchilla C3. Alteration of ME mucosa by pneumococcal neuraminidase and alteration of ME epithelial cell (MEEC) surface carbohydrates during intranasal pneumococcal infection have been demonstrated. Pathogenesis studies have been aided by cultured chinchilla MEEC systems, in which the ability of platelet activating factor and interleukin (IL)-1 beta to stimulate epithelial mucous glycoprotein synthesis has recently been demonstrated. Because chronic OM with effusion is characterized by presence of large amounts of mucous glycoprotein in the ME, pneumococcus may have an important role in both acute and chronic ME disease. Both unconjugated PS and PS-protein-conjugated vaccines are immunogenic after intramuscular administration without adjuvant in chinchillas. Passive protection studies with human hyperimmune immunoglobulin demonstrated that anti-PS IgG alone is capable of protecting the chinchilla ME from direct ME challenge with pneumococci. Active PS immunization studies demonstrated protection fo...

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Neutrophil Oxygen Metabolite Inhibition of Cultured Chinchilla Middle Ear Epithelial Cell Growth

Cited by 3 publications

References 23 publications

New views on the pathogenesis of acute otitis media and its complications

New views on the pathogenesis of acute otitis media and its complications

Early Inflammatory Changes of the Haemophilus influenzae-Induced Experimental Otitis Media

Otitis Media: The Chinchilla Model1

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