传统认为咽鼓管功能不良是慢性中耳渗液的病因。但许多有关研究是在非生理性的条件下作出的,难以令人置信,例如对已有鼓膜穿孔或鼓膜置通气管病人(即已是患病耳)的咽鼓管功能作测量,不能得出中耳渗液前的情况。近年来许多研究向免疫学领域发展,认为免疫反应可能是慢性中耳疾病的主要病因或继发于咽鼓管功能不良。正常情况下,急性中耳渗液通过抗原、抗体和补体之间的免疫反应,渗出物吸收,咽鼓管通畅而治愈。但是,分泌物由于粘滞性增加,粘膜纤毛中毒性损害而不能排出中耳腔,从而处于慢性炎症状态。这可能由于渗液成分之间的比例改变,尤其是可溶性抗原-抗体复合物及补体C_3之间,或者因抗原致敏的上皮细胞与T淋巴细胞之间有选择性的相互作用而释放淋巴因子和产生巨噬细胞侵犯。这一发展,构成Gell和Coombs Traditional Eustachian tube dysfunction that is the etiology of chronic middle ear effusion. However, many studies have been made under non-physiological conditions and are unbelievable. For example, the eustachian tube function of a patient who has a tympanic membrane perforation or tympanic membrane placement (ie, a diseased ear) can not be measured Out of the middle ear effusion before the situation. In recent years, many studies have developed to immunology, that the immune response may be the main cause of chronic middle ear disease or secondary to eustachian tube dysfunction. Under normal circumstances, the acute middle ear effusion through the antigen, antibody and complement between the immune response, exudate absorption, eustachian tube patency and cure. However, the secretions are in a chronic inflammatory state due to increased viscosity and toxic damage to mucociliary cilia that can not be excreted in the middle ear cavity. This may be due to a change in the ratio between exudate components, especially the soluble antigen-antibody complex and complement C_3, or antigen-sensitized epithelial cells and T lymphocytes that selectively interact with each other to release lymphokines And produce macrophage invasion. This development constitutes Gell and Coombs