Clinical implications of inflammatory cytokines in the cochlea: a technical note

Otol Neurotol. 2002 May;23(3):316-22. doi: 10.1097/00129492-200205000-00015.

Abstract

Hypothesis: Establishing the presence of critical cellular stress response components in cochlear cells can contribute to a better understanding of cochlear cell biology and pathology.

Background: Inflammatory cytokines and related proteins play critical roles in a variety of cellular processes, but to date, little is known about the identity and cellular localization of these compounds within the ear. Cytokines are autocrine, which means that cells that produce them have corresponding surface receptors. The presence of these receptors makes the cells vulnerable to disruption by circulating or local sources of cytokines and related ligands. Such disruptions may explain previously poorly understood cochlear pathologies.

Methods: The messenger RNA precursors that encode inflammatory cytokines and related proteins are identified in the inner ear by using reverse transcriptase-polymerase chain reaction. Cochlear cells that contain the corresponding proteins are identified by immunostaining.

Results: Messenger RNA for interleukin-1alpha, tumor necrosis factor alpha, NFkappaB P65 and P50, and IkappaBalpha was found in cochlear tissue. Cells that immunostained most conspicuously for cytokine production are Type I fibrocytes and root cells located within the spiral ligament.

Conclusion: Production of inflammatory cytokines by the above-mentioned cells indicates that they are vulnerable to disruption by extra-cochlear sources of cytokines and associated ligands. These cells play critical roles in cochlear function, and their disruption could induce hearing loss. These findings suggest that systemic or local production of inflammatory ligands may play roles in a number of causes of deafness, including immune mediated hearing loss, sudden hearing loss, and sensorineural hearing loss associated with otosclerosis, otitis media, and bacterial meningitis.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Cochlea / cytology
  • Cochlea / metabolism*
  • Cytokines / genetics
  • Cytokines / metabolism*
  • Guinea Pigs
  • Humans
  • Immunologic Techniques
  • Inflammation Mediators / metabolism*
  • Inflammation Mediators / physiology
  • Male
  • Mice
  • Mice, Inbred CBA
  • RNA, Messenger / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • Staining and Labeling

Substances

  • Cytokines
  • Inflammation Mediators
  • RNA, Messenger