The Role of Inflammatory Mediators in the Pathogenesis of Otitis Media and Sequelae.
- Author:
Steven K JUHN
1
;
Min Kyo JUNG
;
Mark D HOFFMAN
;
Brian R DREW
;
Diego A PRECIADO
;
Nicholas J SAUSEN
;
Timothy T K JUNG
;
Bo Hyung KIM
;
Sang Yoo PARK
;
Jizhen LIN
;
Frank G ONDREY
;
David R MAINS
;
Tina HUANG
Author Information
- Publication Type:Review
- Keywords: Otitis media; Inflammatory mediators; Cytokines; Chemokines; Cholesteatoma; Sensorineural hearing loss
- MeSH: Bacterial Toxins; Chemokines; Cholesteatoma; Cochlea; Cytokines; Ear, Inner; Ear, Middle; Endolymph; Evoked Potentials, Auditory, Brain Stem; Hearing Loss; Hearing Loss, Sensorineural; Homeostasis; Membranes; Models, Animal; Otitis; Otitis Media; Permeability; Recycling; Scala Tympani
- From:Clinical and Experimental Otorhinolaryngology 2008;1(3):117-138
- CountryRepublic of Korea
- Language:English
- Abstract: 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.
