Introduction
Otitis Media of Effusion (OME) is a common multiple disease in E.N.T.
Department, mainly manifested as Middle Ear Effusion (MEE) in the drum
room. Generally, MEE can be diagnosed as OME after the Acute Otitis
Media (AOM) lasts for at least 3 months or has been found to be
asymptomatic during the specialist examination [1]. Allergy has been
reported to increase the incidence of OME by 2-4.5 times compared with
non-allergic people [2-3], and allergic inflammation of the upper
respiratory mucosa may involve in OME pathogenesis [4], suggesting
that there is a correlation between and allergy.
At present, the main causes of OME are mechanical obstruction of the
eustaphylococcal tube, infection, and allergy, among which the mechanism
of allergy is still debated. In recent years, according to the theory of
”consistency of upper and lower respiratory tract inflammation”, ”all
parts of upper and lower respiratory tract are anatomically continuous,
and inflammation is rarely confined to one part. In recent years,
studies on OME pathogenesis have found that innate immunity plays a
protective role in the middle ear. When inflammation occurs, this
protective response is destroyed, resulting in immune imbalance of the
middle ear [5-6]. An increasing number of studies [7-8] have
shown that activation of downstream inflammatory signaling pathways
caused by cellular immunity and some humoral immune factors is a
contributing factor to OME, and is related to immune factors affecting
lymphatic reflux, promoting luminal mucosa swelling and gland secretion,
and thus leading to OME. The mechanism of Th17/Treg cell-mediated immune
response has become the focus of multidisciplinary research
[8-9].However, few studies on Th17 and Treg cells in OME have been
reported. In this study, the role of T cells in OME pathogenesis and its
significance were explored from the perspective that the immune response
induced by Treg/Th17 imbalance may be the cause of OME.