Trauma-induced vestibular dysfunction: Possible functional repair under α1-antitrypsin-rich conditions

Sabri El-Saied, Melodie Zaknoun, Osama Alatawna, Ben Zion Joshua, Noor Kabahaa, Daniel M. Kaplan, Eli C. Lewis

Research output: Contribution to journalArticlepeer-review

Abstract

Transient vestibular organ deafferentation, such that is caused by traumatic tissue injury, is presently addressed by corticosteroid therapy. However, restoration of neurophysiological properties is rarely achieved. Here, it was hypothesized that the tissue-protective attributes of α1-antityrpsin (AAT) may promote restoration of neuronal function. Inner ear injury was inflicted by unilateral labyrinthotomy in wild-type mice and in mice overexpressing human AAT. A 2-week–long assessment of vestibular signs followed. All animals responded with peak vestibular dysfunction scores within 4 h after local trauma. While wild-type animals displayed partial or no recovery across 7 days post-injury, AAT-rich group exhibited early recovery: from behavioral score 9-out-of-9 at peak to 4.8 ± 0.44 (mean ± SD) within 8 h from injury, a time when wild-type mice scored 8.6 ± 0.54 (p < 0.0001), and from vestibular score 15-out-of-15 to 7.8 ± 2.2 within 24 h, when wild-type mice scored 13.0 ± 2.0 (p < 0.01). Thus, recovery and functional normalisation of an injured vestibular compartment is achievable without corticosteroid therapy; expedited tissue repair processes appear to result from elevated circulating AAT levels. This study lays the foundation for exploring the molecular and cellular mediators of AAT within the repair processes of the delicate microscopic structures of the vestibular end organ.

Original languageEnglish
Article number104150
JournalCellular Immunology
Volume356
DOIs
StatePublished - 1 Oct 2020

Keywords

  • Bullostomy
  • Fistula
  • Inflammation
  • Labyrinthotomy
  • Perilymph
  • Tissue injury
  • Vestibular signs

Fingerprint

Dive into the research topics of 'Trauma-induced vestibular dysfunction: Possible functional repair under α1-antitrypsin-rich conditions'. Together they form a unique fingerprint.

Cite this