An animal model for the study of genetic predisposition in the pathogenesis of middle ear inflammation

Objectives: Chronic otitis media with effusion (COME) is the most prevalent inflammatory disease in children and is associated with numerous adverse l ongterm sequelae. Many factors have been associated with an increased risk of developing COME, one of which may be a genetic predisposition to the dis ease. To study the role that genetics play in the pathogenesis of COME, we used an animal model to compare the middle ear inflammatory responses in tw o different strains of rats (Lewis and Fisher). Methods: In earlier studies , we demonstrated that exposure of the middle ear to endotoxin caused early extensive exudation and, later, goblet cell hyperplasia and mucin hypersec retion. In the present study, the animals were divided into six groups. In each group the animals were given transtympanic injection with gram-positiv e bacterial cell wall product (peptidoglycan-polysaccharide [PG-PS]). The m iddle ear bullae were studied at 1 week. and 3 weeks after infection, and a fter systemic reinfection. Comparisons were made of the quantity of mucin e xudate by enzyme-linked immunosorbent assay and by histological evaluation of the middle ear epithelial thickness. Results: Our data demonstrate a sta tistically significant difference in middle ear inflammation and effusion f ormation between the two genetically different strains of rats. Conclusions : These data support the hypothesis that the middle ear response to PG-PS m ay be genetically determined and therefore suggest that genetic predisposit ion may play a role in the pathogenesis of COME.