Trauma–Induced Inner Ear Dysfunction: Functional Repair Under α1-Antitrypsin–Rich Conditions

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 labyrinthectomy 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 dysfucntion scores within 4 hours of local trauma. While wild-type animals displayed partial or no recovery across 7 days post-injury, AAT-rich group exhibited marked recovery within 8-24 hours (behavioral) and 8-48 hours (vestibular), reaching full recovery in the majority of functional measurements by 1 week. Thus, recovery and functional normalisation of an injured vestibular compartment is achievable without corticosteroid therapy; expedited tissue repair processes appear to result from elevated circulting AAT levels. This study lays the foundation for exploring the molecular and cellular mediators of AAT within the repair processes of the delicate microscopic Cochlear structures.