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

Tomiyama, Shunichi; Kinoshita, Toshiyuki; Jinnouchi, Ken; Ikezono, Tetsuo; Gotoh, Yuichi; Pawanker, Ruby; Yagi, Toshiaki

doi:10.1159/000276724

Cited by 16 publications

(8 citation statements)

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“…Experimental endolymphatic hydrops induced by mechanical obliteration of the endolymphatic duct is the best-known and best-studied animal model [Kimura and a b Schuknecht, 1965]. Our previous study showed that secondary antigen challenge to the endolymphatic sac caused endolymphatic hydrops, fluctuating hearing loss, and an increase in the SP/AP ratios on electrocochleograms [Tomiyama et al, 1995]. These findings suggest that a type III allergic reaction in the inner ear induces both morphological and electrophysiological changes that are similar to those observed in Ménière's disease.…”

Section: Discussionmentioning

confidence: 99%

Passive Transfer of Experimental Autoimmune Labyrinthitis

et al. 2000

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The aim of the present study was to establish an animal model of autoimmune labyrinthitis using heterologous inner ear antigen (IEAg) and to elucidate whether the experimentally induced labyrinthitis could be passively transferred. Cochlear and vestibular membranous labyrinthine tissues from bovine temporal bones were used as IEAg. Donor mice were inoculated intracutaneously at multiple sites with an emulsion consisting of equal parts of IEAg and complete Freund’s adjuvant. After 10 days, mononuclear cells were collected from lymph nodes, spleen and blood of the donor mice and injected intravenously into naive recipient mice. Cellular infiltration was observed in the perilymphatic space of the cochlea of all donor and recipient mice. Endolymphatic hydrops was also observed in 63% of donor and 42% of recipient mice. These findings suggest that the experimentally induced labyrinthitis observed in this animal model was probably due to an autoimmune reaction to the IEAg and was passively transferred by a cell-mediated immune raction.

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Section: Discussionmentioning

confidence: 99%

Passive Transfer of Experimental Autoimmune Labyrinthitis

et al. 2000

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“…An immune injury in the ES has been suggested to play an important role in the pathogenesis of MD [Tomiyama et al, 1993[Tomiyama et al, , 1994[Tomiyama et al, , 1995. Recurrent inflammation of the ES leads to fluid homeostasis dysfunction of the inner ear and to conditions that resemble MD [Tomiyama, 1992;Gloddek et al, 1999].…”

Section: Introductionmentioning

confidence: 99%

Experimental Hyperactivity of the Endolymphatic Sac

Friis

Thomsen²,

Poulsen³

et al. 2013

Audiol Neurotol

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Injury to the endolymphatic sac may play an important role in the pathogenesis of Ménière’s disease, an inner ear disorder characterized by hearing loss, tinnitus and attacks of vertigo. Isoimmunization of 16 inbred Lewis rats with a crude endolymphatic sac extract and complete Freund’s adjuvant induced hyperactivity of the endolymphatic sac. One group of rats was immunized by a single dose whereas a second group was immunized twice. Control animals were injected with Freund’s adjuvant in saline only. Serum was collected from all rats by the end of the study and harvested autoantibodies were tested by immunohistochemistry. The endolymphatic sacs were investigated by transmission electron microscopy. Endolymphatic sac stimulation was observed in all immunized rats. Based on detailed ultrastructural observations, the degree of reactivity seemed proportional to the number of injections and the extent of immunization. Moreover, the ribosome-rich cells seemed hyperactive with an extravagant content of intracellular components: numerous rough endoplasmic reticulum and free ribosomes, morphological signs of extensive endo- and exocytosis, vesicles of material with a density similar to the homogeneous substance of which many were observed to fuse with primary lysozymes. Basolateral foldings were numerous and in the subepithelial capillaries formation of multiple and apposing fenestrations were observed. No endolymphatic sac stimulation was observed in the control animals. Specific ribosome-rich cell alterations identical to those present in the endolymphatic sac of Ménière’s disease were observed 21 days after the first immunization. The observations suggest that either an autoantigen or a trophic factor, capable of inducing a hyperactivity of the ribosome-rich cells and an imbalance of the homogeneous substance metabolism, exists in the endolymphatic sac of the rat.

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“…In addition, a few cells were detected in the perilymphatic space of the cochlea, probably as a result of migration from the spiral collecting venules. When we investigated the distribution of injected keyhole limpet hemocyanin (KLH) antigen immunohistochemically, we could not detect antigen in the cochlea, although it was detected in the ES (6). Previous studies have also demonstrated that the spiral modiolar veins developed high endothelial vein-like (HEV-like) characteristics after inoculation of live cytomegalovirus or inactivated virus into the scala tympani of guinea pigs (7).…”

Section: Introductionmentioning

confidence: 82%

Intercellular Adhesion Molecule-1 Expression in the Inner Ear of Rats following Secondary Immune Reaction in the Endolymphatic Sac

Pawankar¹

1998

Acta Oto-Laryngologica

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Pawankar R, Tomiyama S, Jinnouchi K, Ikezono T, Nonaka M, Yagi T. Intercellular adhesion molecule-1 expression in the inner ear of rats following secondary immune reaction in the endolymphatic sac. Acta Otolaryngol (Stockh) 1998; Suppl 539: 5-14.An immunological aetiology for inner ear diseases has long been proposed. The endolymphatic sac (ES) is the only immunoprivileged site in the inner ear with a resident population of immunocompetent cells. By keyhole limpet hemocyanin (KLH) challenge into the ES of systemically pre-immunized guinea pigs, we previously demonstrated an infiltration of inflammatory cells into the perilymphatic space of the cochlea. In order to understand the mechanisms involved in the recruitment of immunocompetent cells into the inner ear, and their relation to the development of endolymphatic hydrops (EH), we investigated the expression and time-kinetics of intercellular adhesion molecule 1 (ICAM-1) in the inner ear of systemically pre-immunized rats after antigen (KLH) challenge into the ES, its relation to cell infiltration in the cochlea and subsequent development of EH. By immunohistochemistry, strong ICAM-1 expression was detected in the spiral ligament, suprastrial region, spiral prominence, spiral modiolar veins, spiral collecting venules, surface membrane of the perilymphatic compartment, perilymphatic space and ES of immunized rats, but not of control rats. ICAM-1 expression was detected at 5-6 h, peaked at 10 -15 h, and gradually reduced by 2 weeks. Cell infiltration into the cochlea started at 6-12 h and peaked at day one. By 6 h, 50% of challenged rats developed EH. This figure rose to 70% at 12 h, and then gradually reduced. However, immunoreactivity for KLH (antigen) was only detected in the ES. These results emphasize that the sac is the central immunological organ of the inner ear, and suggest that ICAM-1 may play a pivotal role in the aetiology of immune-mediated inner ear diseases through the recruitment of immunocompetent cells into the inner ear and subsequent development of EH.

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

Cited by 16 publications

References 11 publications

Passive Transfer of Experimental Autoimmune Labyrinthitis

Passive Transfer of Experimental Autoimmune Labyrinthitis

Experimental Hyperactivity of the Endolymphatic Sac

Intercellular Adhesion Molecule-1 Expression in the Inner Ear of Rats following Secondary Immune Reaction in the Endolymphatic Sac

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