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

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.

Ossicular Chain Lesions in Tympanic Perforations and Chronic Otitis Media without Cholesteatoma

“…This is a remarkable difference with COM, in which we observed BC impairment in presence of OCS [1] . Our hypothesis, supported by histopathological and biological evidence [8,9] , is that differences exist in middle/inner ear interaction between COM and NCOM/TP.…”

Adaptive Immunity in the Middle Ear Mucosa with Chronic Otitis Media

“…At the acute stage, the middle ear epithelial cells respond to infection by the production of cytokines such as IL-8 via the NF-κB signaling pathway [18,19]. IL-8, in turn, attracts the infiltration of neutrophils into the inflammatory site [20]. Bacteria are rapidly killed and infection is usually resolved within 7-10 days in animal models as shown in our previous studies [16,21].…”

“…There are a lot of inflammatory cytokines and inflammatory mediators in middle ear infection as reported previously [20]. Some of these cytokines and inflammatory mediators such as IFNγ and interleukin-6 (IL-6) are critical for COM because they are involved in the regulation of immune and inflammatory responses.…”

HCMV-Encoded UL128 Enhances TNF-α and IL-6 Expression and Promotes PBMC Proliferation Through the MAPK/ERK PathwayIn Vitro

“…Second, CMV promotes the secretion of cytokines and chemokines that act upon these cells. Chronic infection caused by this virus may induce a microenvironment called ''smoldering inflammation,'' which may correlate with the development of many inflammatory disorders (16). CMV infection increases the expression of cytokines such as TNF-a, IL-6, and IL-8 (17,18).…”