Eustachian tube gland tissue changes are related to bacterial species in acute otitis media

Cayé‐Thomasen, Per; Tos, Mirko

doi:10.1016/j.ijporl.2003.09.010

Cited by 9 publications

(5 citation statements)

References 33 publications

(58 reference statements)

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“…Furthermore, the 3D reconstruction of single tubes (Hardisty et al, 2003) may be prone to sample bias. We analyzed multiple tubes and found no change in the overall volume of tube lumen or enlargement of adjacent auditory-tube SMGs that would potentially compress the tube (Cayé-Thomasen and Tos, 2004). We did not recognize overt auditory-tube abnormalities in Fbxo11 Jf/+ mice and infer that bulla adhesions may contribute to the retention of effusion within the bulla cavity of Fbxo11 Jf/+ mice.…”

Section: Discussionmentioning

confidence: 99%

Chronic otitis media is initiated by a bulla cavitation defect in the FBXO11 mouse model

Pozo

MacIntyre

Azar

et al. 2019

Disease Models &Amp; Mechanisms

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Auditory bulla cavitation defects are a cause of otitis media, but the normal cellular pattern of bulla mesenchyme regression and its failure are not well understood. In mice, neural-crest-derived mesenchyme occupies the bulla from embryonic day 17.5 (E17.5) to postnatal day 11 (P11) and then regresses to form the adult air-filled bulla cavity. We report that bulla mesenchyme is bordered by a single layer of non-ciliated epithelium characterized by interdigitating cells with desmosome cell junctions and a basal lamina, and by Bpifa1 gene expression and laminin staining of the basal lamina. At P11-P12, the mesenchyme shrinks: mesenchyme-associated epithelium shortens, and mesenchymal cells and extracellular matrix collagen fibrils condense, culminating in the formation of cochlea promontory mucosa bordered by compact non-ciliated epithelial cells. FBXO11 is a candidate disease gene in human chronic otitis media with effusion and we report that a bulla cavitation defect initiates the pathogenesis of otitis media in the established mouse model Jeff ( Fbxo11 Jf/+ ). Persistent mesenchyme in Fbxo11 Jf/+ bullae has limited mesenchymal cell condensation, fibrosis and hyperplasia of the mesenchyme-associated epithelium. Subsequent modification forms fibrous adhesions that link the mucosa and the tympanic membrane, and this is accompanied by dystrophic mineralization and accumulation of serous effusion in the bulla cavity. Mouse models of bulla cavitation defects are important because their study in humans is limited to post-mortem samples. This work indicates new diagnostic criteria for this otitis media aetiology in humans, and the prospects of studying the molecular mechanisms of murine bulla cavitation in organ culture.

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Section: Discussionmentioning

confidence: 99%

Chronic otitis media is initiated by a bulla cavitation defect in the FBXO11 mouse model

Pozo

MacIntyre

Azar

et al. 2019

Disease Models &Amp; Mechanisms

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“…The absence of auditory tube dilation in Junbo mice may relate to bulla infection/inflammation inducing auditory tube gland enlargement via hypertrophy of the mucous cell population. In the rat, bulla infection causes gland enlargement, narrowing of the auditory tubes and altered mucus composition/viscosity that impairs bulla clearance and prolongs otitis media (33). The accumulation of significantly larger foreign body particles in bullae of HED mutant mice compared to Junbo mice is associated with a heavy foreign body load in the nasopharynx, coupled with a loss of glandular mucus and reduced capacity for particle trapping.…”

Section: Discussionmentioning

confidence: 99%

Ectodysplasin signalling deficiency in mouse models of hypohidrotic ectodermal dysplasia leads to middle ear and nasal pathology

et al. 2016

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Hypohidrotic ectodermal dysplasia (HED) results from mutation of the EDA, EDAR or EDARADD genes and is characterized by reduced or absent eccrine sweat glands, hair follicles and teeth, and defective formation of salivary, mammary and craniofacial glands. Mouse models with HED also carry Eda, Edar or Edaradd mutations and have defects that map to the same structures. Patients with HED have ear, nose and throat disease, but this has not been investigated in mice bearing comparable genetic mutations. We report that otitis media, rhinitis and nasopharyngitis occur at high frequency in Eda and Edar mutant mice and explore the pathogenic mechanisms related to glandular function, microbial and immune parameters in these lines. Nasopharynx auditory tube glands fail to develop in HED mutant mice and the functional implications include loss of lysozyme secretion, reduced mucociliary clearance and overgrowth of nasal commensal bacteria accompanied by neutrophil exudation. Heavy nasopharynx foreign body load and loss of gland protection alters the auditory tube gating function and the auditory tubes can become pathologically dilated. Accumulation of large foreign body particles in the bulla stimulates granuloma formation. Analysis of immune cell populations and myeloid cell function shows no evidence of overt immune deficiency in HED mutant mice. Our findings using HED mutant mice as a model for the human condition support the idea that ear and nose pathology in HED patients arises as a result of nasal and nasopharyngeal gland deficits, reduced mucociliary clearance and impaired auditory tube gating function underlies the pathological sequelae in the bulla.

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“…Caye-Thomasen ve Tos'un, akut otitte bakteri türlerine göre östakiye ait bezlerdeki değişiklikleri inceledikleri araştırmada, bakterinin türünden bağımsız olarak goblet hücresi dansitesinin 6 aya kadar arttığı saptanmıştır. 31 Çalışmamızda, gastrik sıvıya sadece 1 hafta maruz kalınmış olması nedeniyle, östaki borusundaki erken döneme ait değişiklikler izlenmiştir. Sı-çanların östakilerinin nazofarengiyal ve timpanik orifisleri ve sağ/sol kulakları goblet hücresi sayısı açısından kıyaslandığında, gruplar arasında herhangi bir fark saptanmamıştır (Resim 2).…”

Section: Discussionunclassified

“…31 Bu artışta primer olarak bezlerin müköz komponentinin hipertrofisinin etkili olduğu ifade edilmektedir. Bu araştırmada, akut otit sonucunda östakinin aşırı düzeyde artmış olan salgı kapasitesinin, östaki fonksiyonunu bozarak orta kulak hastalığını kötüleştirdiği sonucuna varılmış-tır.…”

Section: Discussionunclassified

The Effects of Gastric Reflux and Artificial Saliva on Eustachian Tube Functions in a Xerostomised Rat Model

Tüz¹,

Aksu²,

Aynali³

et al. 2013

Turkiye Klinikleri J Med Sci

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Eustachian tube gland tissue changes are related to bacterial species in acute otitis media

Cited by 9 publications

References 33 publications

Chronic otitis media is initiated by a bulla cavitation defect in the FBXO11 mouse model

Chronic otitis media is initiated by a bulla cavitation defect in the FBXO11 mouse model

Ectodysplasin signalling deficiency in mouse models of hypohidrotic ectodermal dysplasia leads to middle ear and nasal pathology

The Effects of Gastric Reflux and Artificial Saliva on Eustachian Tube Functions in a Xerostomised Rat Model

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