Immunologic aspects of otitis media.

Immunologic aspects of otitis media.
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DOI:
10.1007/s11882-002-0056-4
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发表时间:
2002-07-01
影响因子:
5.5
通讯作者:
Bernstein, Joel M
Bernstein, Joel M
中科院分区:
医学2区
文献类型:
--
作者:
Bernstein, Joel M

文献摘要

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中耳裂是一种改良的气囊,当气体含量由正常的咽鼓管调节时,其功能正常,导致中耳压力与环境压力平衡。这种中耳压力的最重要的调节器是咽鼓管,它是从鼻咽进入中耳的关键通道。任何由病毒、过敏、污染物引起的咽鼓管粘膜纤毛功能的改变,或鼻咽正常内环境的改变,都会导致咽鼓管阻塞。这反过来又导致中耳通气不足和液体渗出。如果细菌或病毒或病毒-细菌相互作用导致中耳感染性疾病,则作为炎症反应的结果产生免疫反应,允许淋巴细胞和抗原呈递细胞进入中耳粘膜。本文总结了中耳粘膜病毒-细菌炎症反应后中耳的免疫反应。虽然分泌型伊加对于保护鼻咽至关重要,但其在中耳中的功能仍未得到解决。证据有力地表明,IgG 1和IgG 3亚类负责根除中耳病原体。最后,审查的替代方法,以预防中耳炎简要讨论在这个关键时期出现的耐药细菌可用的抗生素。
The middle ear cleft is a modified gas pocket which functions normally when the gas contents are regulated by a normal eustachian tube, resulting in equalization of middle ear pressure to that of the environment. The most important regulator of this middle ear pressure is the eustachian tube, a critical passageway from the nasopharynx into the middle ear. Any alteration of eustachian tube mucociliary function caused by virus, allergy, pollutants, or alteration of the normal homeostasis of the nasopharynx will result in eustachian tube obstruction. This, in turn, leads to underventilation of the middle ear, and transudation of fluid. If bacteria or virus or viral-bacterial interaction leads to infectious disease of the middle ear, an immune response is produced as a result of the inflammatory response, allowing lymphocytes and antigen-presenting cells to enter into the middle-ear mucosa. This article summarizes the immunologic reactivity in the middle ear following a viral-bacterial inflammatory reaction in the middle-ear mucosa. Although secretory IgA is critical for protection of the nasopharynx, its function in the middle ear has still not been resolved. The evidence strongly suggests that IgG1 and IgG3 subclasses are responsible for eradication of middle ear pathogens. Finally, a review of alternative approaches to the prevention of otitis media is briefly discussed in this critical period of emergence of resistant bacteria to available antibiotics.