Experimental Otitis Media with Effusion Induced by Interleukin 2

Kim, Byung Guk; Park, Yong Soo; Jung, Dae Gun; Park, So Young; Yeo, Sang Won; Chae, Sa Yong

Abstract

BACKGROUND AND OBJECTIVES: The etiology and pathogenesis of otitis media with effusion (OME) have not been fully elucidated, although multiple theories exist. These pathogenic factors are eustachian tube dysfunction, allergy, local immune dysfunction and bacterial infection. Recently, many studies have focused on the immune regulation and cytokines associated with the pathogenesis of OME. Interleukin 2 (IL-2) is produced by activated T cells which act on T cells, promoting their proliferation and inducing the production of other cytokines involved in the cell-mediated immunity. This study tested the hypothesis that IL-2 in the middle ear cleft can induce OME and that an IL-2 antagonist can prevent IL-2 induced OME. In addition, we examined histopathological changes in the middle ear.
MATERIALS AND METHODS
IL-2 (group 1: 0.01ng, group 2: 0.1ng) or with its antagonist (group 3: 0.1ng) were injected transtympanically into the middle ear of normal rats.
RESULTS
After 24 hours, IL-2 had produced a cellular effusion (group 1: 75%, group 2: 88%) and histopathological changes including thickening of the subepithelial space and increased infiltration of inflammatory cells. Neutrophils were the predominant cell type. Finally, transtympanic injection of the IL-2 antagonist prevented IL-2 induced OME.
CONCLUSION
This study demonstrated that the IL-2 injection into middle ear can induce OME and that IL-2 antagonist can effectively prevent IL-2 induced OME. These findings suggest that IL-2 plays an important role in the pathogenesis of OME and that the IL-2 antagonist may be applied for the treatment of human OME.