In about one-third of all cases the disease seems to be of autoimmune origin, even though immunological mechanisms involved are not yet obvious [1,2]. INTRODUCTION == Meniere’s disease (MD) is an idiopathic inner ear disorder characterized by fluctuating hearing loss, episodic vertigo and tinnitus in which the histopathological lesion takes the form of endolymphatic hydrops. Vascular disturbances or infectious brokers may be involved in its development, but the etiopathogenesis of the disease is still unknown. In Tolazamide about one-third of all cases the disease seems to be of autoimmune origin, even though immunological mechanisms involved are not yet obvious [1,2]. Recently various groups have focused their attention on the immune response to inner ear antigens and a number of studies have sought to identify these autoantigens. Weiet al. [3] found antibodies reactive with autologous ganglion cells in MD patients, but not in patients with temporal bone trauma. The authors suggested that alterations in the microvascolature due to an autoimmune reaction in the spiral ganglion could trigger MD. Raised levels of anti-collagen II antibodies have also been reported in Tolazamide a high percentage of MD patients by Yooet al. [46], although these Tolazamide findings were not confirmed by others. In 1994 we analysed the levels of antibodies to collagen (C) II, V, I and basement membrane proteins (laminin and CIV) in MD patients, but a clear role of these autoantibodies in the pathogenesis of MD could not be established [7]. Thus, despite many studies the role of antibodies reactive with structures of the inner ear in the pathogenesis of MD remains unsettled. The aim of the present study was to evaluate the reactivity of sera from MD patients with inner ear antigens, and to correlate the serological findings with the clinical manifestations of the disease. == PATIENTS AND METHODS == == Patients == Twenty-five patients affected by Meniere’s disease were analyzed: 11 women and 14 men, aged 3276 years (mean age SD: 5116 138 years). In all patients the disease was monolateral with a period of more than 9 years (mean period SD: 1196 22 years). The diagnosis of MD was made based on the criteria contained in the 1995 Committee on Hearing and Equilibrium Guidelines [8]. The patients were given a thorough audiological examination, including pure firmness audiometry, clinical timpanometry, and brain stem-evoked response audiometry assessments. Vestibular function was assessed by videonystagmography (VNG Ulmer 13 System) to detect the presence of spontaneous nystagmus, positional and positioning nystagmus, and head-shaking nystagmus. The Fitzerald-Hallpike caloric assessments were also performed. In all patients the investigations were carried out in intercritical periods. The patients also underwent brain computerized axial tomography and/or magnetic nuclear resonance scans. Pure firmness audiometry showed sensorineural low frequency hearing loss (LFHL) in 11 (44%) patients and sensorineural smooth hearing loss (FHL) in 14 (56%). The level of hearing loss was assessed by four frequency pure-tone averages (PTA) ranging from 500 to 3000 Hz. No cases of high frequency hearing loss were disclosed. The Auditory Evoked Brainstem Tolazamide Responses test (AEBR) confirmed Rabbit Polyclonal to p300 the cochlear origin of the hearing loss. Videonystagmography showed positional nystagmus in 7 patients. Head-shaking nystagmus (HSN) was positive in 11 cases and the caloric test revealed canal paresis in all patients. After their informed consent was obtained, serum samples were taken and immediately stored at 20C. Sera from 38 healthy donors (18 women, 20 men, age 2575, mean age SD: 40 12 years) were used as controls. No one suffered from otologic disorder or systemic autoimmune diseases. All sera were tested for antibodies to inner ear, spleen and liver antigens and for non-organ specific antigens. == Isolation of inner ear == Inner ear material was isolated from new bovine Tolazamide temporal bones obtained from a local abattoir. Temporal bone microdissection was carried out using a median approach following the petrous ridge and internal auditory canal. After the dura was removed from the temporal bone, the superior portion of the internal auditory canal was drilled, and the basal change of the cochlea was sought for immediately beneath the.