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II型胶原介导的自身免疫性中耳疾病:咽鼓管疾病、分泌性中耳炎和鼓室硬化症。

Type II collagen mediated autoimmune middle ear disease: eustachian tube disease, otitis media with effusion and tympanosclerosis.

作者信息

Yoo T J, Sudo N, Tomoda K, Yazawa Y, Ishibe T, Takeda T, Floyd R

出版信息

Auris Nasus Larynx. 1985;12 Suppl 1:S91-3. doi: 10.1016/s0385-8146(85)80112-7.

Abstract

Intact Eustachian tube and tympanic cavity functions are essential for normal middle ear physiology. Type II collagen is an essential component of ear tissue. Autoimmune response to this type II collagen produces sensorineural hearing loss, vestibular dysfunction, endolymphatic hydrops, otospongiosis-like lesions, Eustachian tube inflammation and Eustachian tube chondritis. In addition, these autoimmune responses occasionally produce otitis media with effusion (not infectious). Tympanosclerosis, which is a frequent sequelae of otitis media with effusions, was also induced by type II collagen immunization together with surgical incision of the tympanic membrane. The exact mechanisms of this type II collagen autoimmune mediated middle ear disease are not clear. However, the animals thus induced have higher antibody titers and cell mediated immune responses to type II collagen. The tympanic membrane showing tympanosclerosis also had C3 and Ig deposits. All the animals with otitis media with effusion induced by type II collagen immunization also had Eustachian tube disease. This could be due to a malfunction of the Eustachian tube. Thus, this model might provide a rational approach for the study of otitis media with effusion associated with vasculitis. Further studies are needed to elucidate the immunologic mechanism involved in the pathogenesis of otitis media with effusion.

摘要

咽鼓管和鼓室功能完整对正常中耳生理至关重要。II型胶原蛋白是耳部组织的重要组成部分。针对这种II型胶原蛋白的自身免疫反应会导致感音神经性听力损失、前庭功能障碍、内淋巴积水、耳海绵样病变、咽鼓管炎症和咽鼓管软骨炎。此外,这些自身免疫反应偶尔会导致分泌性中耳炎(非感染性)。鼓膜硬化是分泌性中耳炎常见的后遗症,II型胶原蛋白免疫接种并联合鼓膜手术切开也可诱发。这种II型胶原蛋白自身免疫介导的中耳疾病的确切机制尚不清楚。然而,如此诱导的动物对II型胶原蛋白具有更高的抗体滴度和细胞介导的免疫反应。出现鼓膜硬化的鼓膜也有C3和Ig沉积。所有由II型胶原蛋白免疫接种诱发分泌性中耳炎的动物也患有咽鼓管疾病。这可能是由于咽鼓管功能失调所致。因此,该模型可能为研究与血管炎相关分泌性中耳炎提供一种合理的方法。需要进一步研究以阐明分泌性中耳炎发病机制中涉及的免疫机制。

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