FAILURE OF ELEVATED HEAT-SHOCK-PROTEIN-70 ANTIBODIES TO ALTER COCHLEAR FUNCTION IN MICE

Heat shock protein 70 (HSP70) has been suggested as the putative cochl ear antigen underlying a proposed autoimmune etiology in certain cases of Meniere's disease and idiopathic hearing loss. To determine if ant ibodies to this cellular protein are capable of altering cochlear func tion, BALB/c (N = 3) and CBA/J (N = 9) mice were inoculated with bovin e HSP70 by intraperitoneal injections (10 mu g in Saline) every 10 day s for 7 or 10 months, respectively. An equal number of control mice we re injected with PBS according to the same schedule. ABR thresholds at 4, 8, 16, and 32 kHz in the HSP70-inoculated mice did not change over the 10 month period and were similar to saline controls. Furthermore, serum immune complexes and antinuclear antibodies did not increase ov er the inoculation period. ELISA analysis demonstrated the mice create d antibodies to the foreign HSP70, but these apparently caused no abno rmalities in the auditory or immune systems. It was concluded that for eign HSP70 is antigenic and inoculation with it will raise antibodies, but these antibodies were neither immunopathogenic nor cochleopathic. Therefore, these findings do not support current theories that elevat ed anti-HSP70 antibodies are the underlying cause of hearing loss in p atients with such antibodies present. (C) 1998 Elsevier Science B.V.