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Kariem Sharaf1, Friedrich Ihler, Mattis Bertlich

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Summary
This summary is machine-generated.

Tumor necrosis factor (TNF) can decrease cochlear blood flow. Both Etanercept and JTE-013 treatments effectively reversed this decrease, suggesting potential therapeutic targets for hearing loss.

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Area of Science:

  • Otolaryngology
  • Immunology
  • Pharmacology

Background:

  • Sudden sensorineural hearing loss is a significant cause of disability.
  • Inflammation and impaired cochlear blood flow (CBF) are implicated in inner ear disorders.
  • Tumor necrosis factor (TNF) is a key mediator of inflammation and microcirculation in the cochlea, with S1P acting downstream.

Purpose of the Study:

  • To quantify the effects of Etanercept (a TNF inhibitor) and JTE-013 (a sphingosine-1-phosphate receptor 2 antagonist) on cochlear blood flow.
  • To investigate the potential of these agents in reversing TNF-induced decreases in cochlear blood flow.

Main Methods:

  • Cochlear lateral wall vessels in guinea pigs were surgically exposed and observed using intravital microscopy.
  • Animals were divided into four groups, receiving TNF superfusion followed by Etanercept, JTE-013, or vehicle.
  • Changes in cochlear blood flow were measured after treatment administration.

Main Results:

  • TNF significantly decreased cochlear blood flow (p < 0.001).
  • Both Etanercept and JTE-013 treatments significantly reversed the TNF-induced reduction in CBF (p < 0.001).
  • No significant difference was observed between vehicle groups or between the two treatment groups.

Conclusions:

  • Etanercept and JTE-013 effectively counteract the negative effects of TNF on cochlear blood flow.
  • TNF and the S1P signaling pathway represent potential therapeutic targets for treating hearing loss associated with microcirculation impairment.