Clin Exp Otorhinolaryngol.  2008 Sep;1(3):117-138. 10.3342/ceo.2008.1.3.117.

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

Affiliations
  • 1Department of Otolaryngology, University of Minnesota Medical School, Minneapolis, MN, USA. juhnx001@umn.edu
  • 2Department of Otolaryngology, Loma Linda University, Loma Linda, CA, USA.

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.

Keyword

Otitis media; Inflammatory mediators; Cytokines; Chemokines; Cholesteatoma; Sensorineural hearing loss

MeSH Terms

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
Bacterial Toxins
Chemokines
Cytokines

Figure

  • Fig. 1 Pathogenesis of otitis media.

  • Fig. 2 Schematic representation of the Id1-induced cellular hyperproliferation and abundant keratin 10 production pathways in keratinocytes. CD1: cyclin D1; Cdks: cyclin-dependent kinases (cdks 4/6); Rb: retinoblastoma; Rb-P: phosphorylated Rb; E2F: a transcription factor that drives the Go/G1-to-S phase transition of cells.

  • Fig. 3 Pathological effects of inflammatory mediators in otitis media.


Cited by  3 articles

Pathogenesis and Bone Resorption in Acquired Cholesteatoma: Current Knowledge and Future Prospectives
Mahmood A. Hamed, Seiichi Nakata, Ramadan H. Sayed, Hiromi Ueda, Badawy S. Badawy, Yoichi Nishimura, Takuro Kojima, Noboru Iwata, Ahmed R. Ahmed, Khalid Dahy, Naoki Kondo, Kenji Suzuki
Clin Exp Otorhinolaryngol. 2016;9(4):298-308.    doi: 10.21053/ceo.2015.01662.

Cytokeratin 13, Cytokeratin 17, and Ki-67 Expression in Human Acquired Cholesteatoma and Their Correlation With Its Destructive Capacity
Mahmood A. Hamed, Seiichi Nakata, Kazuya Shiogama, Kenji Suzuki, Ramadan H. Sayed, Yoichi Nishimura, Noboru Iwata, Kouhei Sakurai, Badawy S. Badawy, Ken-ichi Inada, Hayato Tsuge, Yutaka Tsutsumi
Clin Exp Otorhinolaryngol. 2017;10(3):213-220.    doi: 10.21053/ceo.2016.01263.

Expression of Prostaglandin E2 Receptors in Acquired Middle Ear Cholesteatoma
Sujie Wang, Li Xie, Yanfei Zhang, Pengfei Xu, Aiguo Liu
Clin Exp Otorhinolaryngol. 2018;11(1):17-22.    doi: 10.21053/ceo.2017.00304.


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