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Can You Hear Me Now? a Genetic Model of Otitis Media with Effusion

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Can You Hear Me Now? a Genetic Model of Otitis Media with Effusion Can you hear me now? A genetic model of otitis media with effusion Evelyn Lazaridis, James C. Saunders J Clin Invest. 2008;118(2):471-474. https://doi.org/10.1172/JCI33716. Commentary Otitis media with effusion (OME) is characterized by the occurrence of fluid in the middle-ear cavity in the absence of any signs of acute ear infection and occurs most frequently in children with auditory or eustachian tube dysfunction. Its chronic form is an important clinical issue for pediatricians and otologists alike. The study by Depreux et al. in this issue of the JCI shows that absence of the transcriptional activatorE ya4 in knockout mice results in abnormal structuring of the eustachian tube, thus predisposing these animals to OME (see the related article beginning on page 651). The development of this genetics-based animal model is an important advance for understanding OME and for exploring new avenues of treatment. Find the latest version: https://jci.me/33716/pdf commentaries Can you hear me now? A genetic model of otitis media with effusion Evelyn Lazaridis and James C. Saunders Department of Otorhinolaryngology, Head and Neck Surgery, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Otitis media with effusion (OME) is characterized by the occurrence of fluid ear cavity. Impairment of cavity ventilation in the middle-ear cavity in the absence of any signs of acute ear infection and drainage is the primary mechanism and occurs most frequently in children with auditory or eustachian tube that triggers an OME episode. In addi- dysfunction. Its chronic form is an important clinical issue for pediatri- tion, the clearance of middle-ear secretions cians and otologists alike. The study by Depreux et al. in this issue of the JCI depends on the integrity of the respiratory shows that absence of the transcriptional activator Eya4 in knockout mice epithelium, in particular, the effectiveness results in abnormal structuring of the eustachian tube, thus predisposing of the ciliated cells in moving secretions. these animals to OME (see the related article beginning on page 651). The Furthermore, craniofacial abnormalities, development of this genetics-based animal model is an important advance of which a palatal defect is one example, for understanding OME and for exploring new avenues of treatment. are also related to a higher incidence of OME because they impair the ET venting In humans, fluid accumulation in the The ET serves two major functions. First, it mechanism (3). middle-ear cavity, in the absence of acute permits air to enter or leave the middle-ear When middle-ear ventilation is impaired, ear infection, is known as otitis media with cavity, thus balancing middle-ear pressure negative middle-ear pressure results, caus- effusion (OME) (1–3). The disorder occurs with ambient air pressure (4). The tensor ing tympanic membrane retraction and most frequently in children, with approxi- veli palatini muscle is primarily responsible the accumulation of middle-ear secretions. mately 2.2 million episodes diagnosed each for active dilatation of the ET, and pressure Notably, the longer these secretions remain year in the United States (2, 3). Fortunately, equilibration occurs most frequently dur- in the cavity, the more likely it is that they spontaneous resolution occurs within three ing swallowing. Second, the ET provides a will produce structural alterations such as months in a large number of these children. conduit through which middle-ear secre- polyp formation, tissue fibrosis, additional Unfortunately, an equally large number of tions can be swept into the nasopharynx, ET obstruction, and, eventually, chronic children have recurrent OME (1). Recur- via the beating action of the ciliated cells. OME (with the so-called “glue ear” condi- rent OME is accompanied by an increased Secretions in the middle ear can arise from tion; ref. 3). The majority of cases of OME risk for sustained conductive hearing loss, two sources: capillary effusion (also called are asymptomatic, but in some children, with the potential for speech, language, transudate effusions; ref. 3), and mucus mild intermittent ear pain, fullness, irrita- and learning problems. The treatment of released into the middle-ear cavity from the bility, ear rubbing, balance problems, a con- chronic OME is thus an important clinical secretory cells of the respiratory epithelium. ductive hearing loss of 25–40 decibels (dB), issue for pediatricians and otologists. Herein, we refer to these secretions collec- delayed language or speech development, The most important factor associated tively as middle-ear secretions. In addition, and/or problems with school performance with OME is abnormal structure and func- reflux through the ET can draw nasophar- may emerge (1). Spontaneous resolution of tion of the eustachian tube (ET) (3). The ET ynx secretions into the middle-ear cavity. OME is largely determined by the original is an osteocartilaginous tube that connects cause and the duration of fluid in the middle the middle-ear cavity to the nasopharynx. Human OME ear but most frequently occurs within three The cartilaginous portion opens into the Immature development of the ET impairs months. The only effective treatment for nasopharynx at the torus tubarius, and the the venting function and increases the chronic OME at present is a tympanostomy osseous portion opens into the anterior likelihood of secretion accumulation in with tube insertion (1). This limited option wall of the middle-ear cavity at the ostium the middle-ear cavity. Other impairments for clinically treating chronic OME, and the (3) (Figure 1A). The lumen of the ET and to the ET can also cause accumulation of difficulty in identifying new treatment pro- the inner surface of the middle-ear cavity these secretions. At the torus tubarius, for cedures, due to the requirement for large are lined with the respiratory epithelium. example, ET obstruction can occur from studies involving children who are at risk for The mucosal layer of the respiratory epithe- hypertrophied adenoids or edema of the structural damage to the ear, calls attention lium consists of secretory cells, ciliated cells, surrounding epithelium (Figure 1, A and B). to the need for an animal model in which supporting cells, and connective tissue (3). At the ostium, the presence of a cholestea- new treatments for OME can be tested. toma (a benign skin growth) or a polyp may Nonstandard abbreviations used: ET, eustachian block the opening of the ET (Figure 1C). In A genetic basis for OME tube; Eya4, eyes absent 4 homolog; OME, otitis media addition, ET dysfunction can be caused by Recently, a new transcriptional activator with effusion. failure of the tube to close, a flaccid tube, was identified in the vertebrate eyes absent Conflict of interest: The authors have declared that no conflict of interest exists. or an inflamed epithelium (Figure 1D). The gene family, called eyes absent homolog 4 Citation for this article: J. Clin. Invest. 118:471–474 net effect of all these examples is blockage (EYA4) (5). This transcriptional activa- (2008). doi:10.1172/JCI33716. of the flow of secretions from the middle- tor plays a developmental role in the early The Journal of Clinical Investigation http://www.jci.org Volume 118 Number 2 February 2008 471 commentaries Figure 1 ET physiology. (A) The normal ET. The ET, which joins the nasopharynx at the torus tubarius and joins the middle-ear cavity at the ostium, permits airflow between the middle-ear cavity and nasopharynx, balancing middle-ear pressure with ambient air pressure. Also, middle-ear secretions are swept into the nasopharynx (clearance) from the middle-ear cavity. (B) Mechanical obstruction of the ET may occur at the torus tubarius by adenoid hypertrophy or edema (B), or at the ostium in the middle-ear cavity by perhaps a polyp or a cholesteatoma (C). The patholo- gies shown in B or C block air flow and the clearance of middle-ear cavity secretions though the ET, increasing middle-ear negative pressure (P–) and accumulation of middle-ear secretions. An intrinsic ET obstruction may also result from epithelium inflammation (D), secondary to nasal infection or allergy. This also results in middle-ear negative pressure and secretion accumulation. TM, tympanic membrane. stages of normal embryogenesis, as it inter- mals had OME. The existence of a genetic was narrower and abnormally positioned acts with proteins in the regulatory hierar- basis for OME has been previously sug- in the middle ear, and 10% of mutant ani- chy. In addition, it is also important in the gested, as the incidence of OME has been mals had a mechanical obstruction of the development of structures within the inner shown to be higher in twin siblings (3); ostium by a polyp (Figure 2). The medial ear, such as the cochlear capsule, Reissner but in their current study Depreux et al. osseous segment was also abnormally nar- membrane, stria vascularis, and the sensory propose that deletion of a specific gene, row in Eya4–/– mice compared with WT epithelia of the vestibular system. EYA4 Eya4, causes OME (6). Auditory brain- mice. Furthermore, there was delayed pala- mutations in humans are related to post- stem responses of the Eya4–/– mice studied tal maturation, which was resolved within lingual, autosomal dominant, progressive revealed a substantial loss in peripheral four weeks, and cilia cell density in the mid- hearing loss at the DFNA10 locus (5). auditory function; however, how much dle-ear cavity was reduced after 16 months Eya4-deficient mice (Eya4–/– mice) appear of this was attributable to the middle-ear in Eya4–/– mice. Table 1 compares and con- to primarily suffer from disrupted ET conductive system is unknown. The inves- trasts the phenotypes of Eya4–/– mice and morphology. It may be the case that EYA4 tigators also excluded the possibility of human infants with OME, revealing that mutations in humans result in abnormal their results arising from middle-ear or ET many of the major characteristics of OME anatomy in the middle ear that contrib- infection by treating pups with antibiotic in children and the Eya4–/– mutant mice utes to the formation of a cholesteatoma.
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