Endolymphatic Hydrops Induced by Immune Response of the Endolymphatic Sac: Relation to Perilymph Antibody Levels

Tomiyama, Shunichi

doi:10.1177/0003489492101s1010

Cited by 26 publications

(19 citation statements)

References 13 publications

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“…Altermatt et al [1990] demonstrated the presence of MHC class II in the normal human endolymphatic sac directly, using anti-MHC-class-II antibodies. This is consistent with the observation that reaction to foreign substances and viruses occurs preferentially in the endolymphatic sac, inducing endolymphatic hydrops after repeated inflammation [Tomiyama and Harris, 1987;Gloddek and Harris, 1989;Tomiyama, 1992]. However, there is evidence from experimental and clinical data that immunological reactions of the inner ear are not always associated with endolymphatic sac involvement [Hughes et al, 1988;Veldman, 1997].…”

Section: Introductionsupporting

confidence: 88%

Induction of MHC Class II Antigens on Cells of the Inner Ear

et al. 2002

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Growing evidence supports the concept that immune reactions occur in the cochlea, where they can function either in protection or as a source of inflammation. Since immunity is generally initiated by antigen presentation of foreign substances to T cells, antigen-presenting cells expressing major histocompatibility complex (MHC) class II molecules are required. Under resting conditions, cochlear cells usually express no MHC class II. However, we show that exposure to γ-interferon in vitro induces an increase in MHC class II expression in neonatal cochlear cells of mice. In addition, MHC class II immunoreactivity was observed in the inner ear of adult mice after induction of sterile labyrinthitis in vivo. It is concluded that the induction of MHC class II molecules by inflammation may render cochlear cells competent to initiate and participate in immune reactions and may therefore contribute to both immunoprotective and immunopathological responses of the inner ear.

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Section: Introductionsupporting

confidence: 88%

Induction of MHC Class II Antigens on Cells of the Inner Ear

et al. 2002

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“…Previous immunological studies of progressive sensorineural hearing loss have suggested that an immunological mechanism may be involved in the development of endolymphatic hydrops, although an inner ear target antigen has yet to be described [7] . McCabe [8] was the first to propose an immunological pathogenetic mechanism for endolymphatic hydrops.…”

Section: Discussionmentioning

confidence: 99%

A Comparison of the Short-Term Outcome in Patients with Acute Low-Tone Sensorineural Hearing Loss

Morita

Suzuki

Iizuka³

2010

ORL

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Purpose of the Study: We aimed to compare the short-term outcome of patients with acute low-tone sensorineural hearing loss (ALHL) treated with steroid alone, diuretics alone or combination treatment. Procedures: Between April 2000 and March 2009, we retrospectively reviewed the medical records of 156 patients with a diagnosis of ALHL. All patients were followed up until improvement or for 8 weeks from the initial examination. Patients were treated with steroid alone (n = 49), diuretics alone (n = 40), combination treatment (n = 46) or they received neither steroid nor diuretics (n = 21). Results: The steroid-diuretic combination therapy for ALHL showed significantly better results than the steroid or diuretic treatments alone (p < 0.05). There were no clinically significant differences in the outcome between the steroid- and diuretic-alone treatments. Conclusion and Message: The etiology of ALHL is described as both an endolymphatic hydrops and an autoimmunological mechanism so that, as expected, the steroid-diuretic combination therapy was more effective than the steroid or diuretic treatments alone.

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“…We previously demonstrated that elevation of peri lymph antibody levels in the early phase was due to an influx of serum but not due to antibody production in the endolymphatic sac [7], Following the type III immune reaction in the endolymphatic sac, acute inflammatory cellular infiltration gradually occurred in the endolym phatic sac from 5 h after antigen challenge and reached a maximum at 12 h. This severe inflammatory reaction per sisted for 3 days and was gradually followed by infiltration of plasma cells and lymphocytes [9]. These findings sug gest that a type III immune reaction can induce an increased vascular permeability of the inner ear.…”

Section: Discussionmentioning

confidence: 98%

Fluctuating Hearing Loss following Immune Reaction in the Endolymphatic Sac of Guinea Pigs

Tomiyama

Kinoshita²,

Jinnouchi³

et al. 1995

ORL

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This study has investigated immune injuries to the inner ear auditory system of guinea pigs. Following secondary antigen challenge to the endolymphatic sac, the mean hearing threshold significantly increased in the early phase from day 1 to day 3 and thereafter recovered. In the early phase, hearing threshold significantly increased simultaneously to the elevation of perilymph antibody levels. The size of hydrops was not the only factor that causes an increase in hearing loss as well as in AP/SP ratio. Scale-out hearing loss was seen in 2 animals with severe degeneration of the stria vascularis as well as the organ of Corti associated with the inflammatory cellular infiltration especially in the perilymphatic space, even in the absence of keyhole limpet hemocyanin antigen in the cochlea. On the other hand, control animals did not suffer hearing loss. These results suggest that an immune reaction in the endolymphatic sac is a possible pathogenic etiology of Ménière’s disease or sudden deafness.

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Endolymphatic Hydrops Induced by Immune Response of the Endolymphatic Sac: Relation to Perilymph Antibody Levels

Cited by 26 publications

References 13 publications

Induction of MHC Class II Antigens on Cells of the Inner Ear

Induction of MHC Class II Antigens on Cells of the Inner Ear

A Comparison of the Short-Term Outcome in Patients with Acute Low-Tone Sensorineural Hearing Loss

Fluctuating Hearing Loss following Immune Reaction in the Endolymphatic Sac of Guinea Pigs

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