Preventing Ototoxic Synergy of Prior Noise Trauma during Aminoglycoside Therapy
Abstract
We have successfully identified two molecular targets among a handful candidates that may contribute to an escalated inner ear ototoxicity. One is the Duffy antigen receptor for chemokines (Darc), and the other is the transient receptor potential vanilloid 1 (TrpV1). Both receptors actively participate in the process of cochlear inflammation, a condition resulting from exposure to moderate and intense noise stimulation. If the pathophysiological condition is quickly resolved, cochlear inflammation does not necessarily result in functional damage. However, the cochleas permeability to circulating substances, especially, ototoxic aminoglycoside medications, is increased during an inflammatory episode, which can escalate the degree of ototoxic damage. Overall, we are getting very close to the goal of this project, to search countermeasures to prevent aminoglycoside-induced cochleotoxicity (and vestibulotoxicity) that can severely debilitate the recovery of military personnel, as well as civilians received aminoglycoside therapy with a history of acoustic insult.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jun 01, 2019
- Accession Number
- AD1094626
Entities
People
- Hongzhe Li
Organizations
- VA Boston Healthcare System