Research in my laboratory is focused on two areas of autoimmune inner ear disease: how systemic immune diseases cause hearing loss and how steroid treatments reverse it. Many patients with hearing disorders (Meniere's disease, sudden hearing loss, autoimmune inner ear disease) have elevated serum immune complexes, but the immune mechanisms causing their hearing loss are unclear. Current research interests are the molecular targets of these circulating autoantibodies and the cellular and molecular processes in the ear that are subsequently compromised. Findings show that circulating autoantibodies disrupt the stria vascularis blood-labyrinth barrier, which interferes with normal transport of potassium into the endolymph and causes loss of the endocochlear potential.

A second research interest is the cellular processes in the cochlea that are responsive to steroid therapy. Current dogma holds that autoimmune disease causes the inner ear to become inflamed and glucocorticoid (prednisone, methylprednisolone) treatments are effective because of their anti-inflammatory and immune suppressive actions. However, because the stria vascularis is responsible for moving potassium ions into the endolymph, it is possible the glucocorticoids are effective because of their sodium transport effects and not their immune suppressive actions. Our research has shown that the mineralocorticoids (aldosterone, fludrocortisone), which only transport sodium and potassium ions and have no immune suppressive actions, are just as effective as the glucocorticoids in reversing or preventing autoimmune inner ear disease. Also, glucocorticoids and mineralocorticoids given in combination are effective at doses lower than those required when given alone. Thus, if alternative steroid treatments can be developed that effectively control hearing loss without the severe side effects of glucocorticoids, long-term management of autoimmune inner ear disease will be possible.

Maccabee, M., Trune, Hwang, P. Effects of topically applied biomaterials on paranasal sinus mucosal regeneration. American Journal of Rhinology, 17:203-7, 2003.

Gross, N.D., Kempton, J. B., Trune, D.R. Spironolactone blocks glucocorticoid mediated hearing preservation in autoimmune mice. Laryngoscope, 112:298-303, 2002.

Trune, D.R., Kempton, J.B. Female MRL.MpJ-Fas^lpr autoimmune mice have greater hearing loss than males. Hearing Research, 167:170-4, 2002.

Pillers, D.M., Kempton, J.B., Duncan, N.M., Pang, J., Dwinnel, S.J., Trune, D.R., Hearing loss in the laminin-deficient dy mouse model of congenital muscular dystrophy. Molecular Genetics and Metabolism, 76:217-24, 2002.

Trune, D.R., J.B. Kempton. Aldosterone and prednisolone control of auditory dysfunction in MRL/MpJ-Fas^lpr autoimmune mice. Hearing Research, 155:9-20, 2001.

Trune, D.R. Mouse models for immunologic diseases of the auditory system. Chapter 33 in: Willott, J.F. (Ed.) Handbook of Mouse Auditory Research: From Behavior to Molecular Biology. CRC Press, 2001.