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

Kawana, Masahiro

doi:10.1016/s0385-8146(12)80104-0

Cited by 9 publications

(4 citation statements)

References 14 publications

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“…Neutrophils have been shown to be associated with the pathogenesis of not only acute OM but also chronic OME in children ( 170 ). Lysozyme accumulation in MEE preceded significant inflammatory cell influx with lysozyme present at 6 hr and inflammatory cells present after 12 hr in MEE in H. influenzae -induced experimental OM ( 171 ). The predominant cell populations in the mucosa and MEEs in COME are mononuclear cells, macrophages, and lymphocytes, with plasma and mast cells also present ( 172 - 176 ).…”

Section: Inflammation and Ommentioning

confidence: 99%

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

Juhn

Jung

Hoffman

et al. 2008

Clin Exp Otorhinolaryngol

139

148

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This review deals with the characteristics of various inflammatory mediators identified in the middle ear during otitis media and in cholesteatoma. The role of each inflammatory mediator in the pathogenesis of otitis media and cholesteatoma has been discussed. Further, the relation of each inflammatory mediator to the pathophysiology of the middle and inner ear along with its mechanisms of pathological change has been described. The mechanisms of hearing loss including sensorineural hearing loss (SNHL) as a sequela of otitis media are also discussed. The passage of inflammatory mediators through the round window membrane into the scala tympani is indicated. In an experimental animal model, an application of cytokines and lipopolysaccharide (LPS), a bacterial toxin, on the round window membrane induced sensorineural hearing loss as identified through auditory brainstem response threshold shifts. An increase in permeability of the blood-labyrinth barrier (BLB) was observed following application of these inflammatory mediators and LPS. The leakage of the blood components into the lateral wall of the cochlea through an increase in BLB permeability appears to be related to the sensorineural hearing loss by hindering K+ recycling through the lateral wall disrupting the ion homeostasis of the endolymph. Further studies on the roles of various inflammatory mediators and bacterial toxins in inducing the sensorineumral hearing loss in otitis media should be pursued.

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Section: Inflammation and Ommentioning

confidence: 99%

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

Juhn

Jung

Hoffman

et al. 2008

Clin Exp Otorhinolaryngol

139

148

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“…We recently observed that interleukin (IL)-lß, IL-6, IL-8, and tumor necrosis factor (TNF) a were detected in MEF of type 3 Spneumoniae-induced experimental otitis media in the chinchilla model with commercially available human enzyme-linked immunosorbent assay (ELISA) kits. 10 We have been investigating the pathophysiology in the middle ear after inoculation of// influenzae 23 and M catarrhalis 24 with a similar procedure, which has been recognized as a significant animal otitis media model. We therefore sought to investigate the course of cytokines of experimentally created MEF using commercially available human ELISA kits in the guinea pig model of otitis media induced by nonviable H influenzae.…”

Section: Introductionmentioning

confidence: 99%

Course of IL-1β, IL-6, IL-8, and TNF-α in the Middle Ear Fluid of the Guinea Pig Otitis Media Model Induced by Nonviable Haemophilus Influenzae

Sato¹,

Kawana²,

Nonomura³

et al. 1999

Ann Otol Rhinol Laryngol

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To characterize the local response in acute otitis media, courses of interleukin (IL)-1beta, IL-6, IL-8, and tumor necrosis factor (TNF)alpha in middle ear fluid (MEF) of the guinea pig otitis media model induced by nonviable Haemophilus influenzae were investigated with enzyme-linked immunosorbent assay (ELISA) kits. The IL-1beta concentration in H. influenzae-inoculated ears peaked 24 hours after inoculation. The IL-8 concentration was significantly higher in H. influenzae-inoculated ears than in controls 48 and 96 hours after inoculation. The TNF-alpha concentration in H. influenzae-inoculated ears had an initial peak 6 hours after inoculation and had significant late increases 48 and 96 hours after inoculation. The results suggest that IL-1beta and TNF-alpha were produced by middle ear mucosa in the early stage of the experiment by stimulation of bacterial inoculation, which caused subsequent inflammatory cell accumulation, and that IL-8 and TNF-alpha were produced in the late stage by accumulating inflammatory cells.

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“…Lysozyme rapidly accumulates within the MEE, within 6 h of experimental NTHi infection. Accumulation of lysozyme occurs approximately 6 h before inflammatory cell influx in the guinea pig model (Kawana, 1995). Furthermore, MEE concentrations of lysozyme are higher in children with mucoid OM compared to children experiencing serous OM (Harada et al, 1990;Liu et al, 1975), and lysozyme secretion was localized to middle ear goblet cells in children .…”

Section: Lysozymementioning

confidence: 92%

Middle Ear and Eustachian Tube Mucosal Immunology

et al. 2015

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

Cited by 9 publications

References 14 publications

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

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

Course of IL-1β, IL-6, IL-8, and TNF-α in the Middle Ear Fluid of the Guinea Pig Otitis Media Model Induced by Nonviable Haemophilus Influenzae

Middle Ear and Eustachian Tube Mucosal Immunology

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