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An Animal Model for the Study of Genetic Predisposition in the Pathogenesis of Middle Ear Inflammation
Author(s) -
Madison Clark J.,
Brinson George,
Newman Michael K.,
Jewett Brian S.,
Sartor Balfour R.,
Prazma Jiri,
Pillsbury Harold C.
Publication year - 2000
Publication title -
the laryngoscope
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.181
H-Index - 148
eISSN - 1531-4995
pISSN - 0023-852X
DOI - 10.1097/00005537-200009000-00019
Subject(s) - middle ear , pathogenesis , otitis , genetic predisposition , effusion , mucin , inflammation , immunology , pathology , disease , biology , medicine , genetics , anatomy , surgery
Objectives Chronic otitis media with effusion (COME) is the most prevalent inflammatory disease in children and is associated with numerous adverse long‐term sequelae. Many factors have been associated with an increased risk of developing COME, one of which may be a genetic predisposition to the disease. 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 two 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 hypersecretion. In the present study, the animals were divided into six groups. In each group the animals were given transtympanic injection with gram‐positive bacterial cell wall product (peptidoglycan‐polysaccharide [PG‐PS]). The middle ear bullae were studied at 1 week and 3 weeks after infection, and after systemic reinfection. Comparisons were made of the quantity of mucin exudate by enzyme‐linked immunosorbent assay and by histological evaluation of the middle ear epithelial thickness. Results Our data demonstrate a statistically significant difference in middle ear inflammation and effusion formation between the two genetically different strains of rats. Conclusions These data support the hypothesis that the middle ear response to PG‐PS may be genetically determined and therefore suggest that genetic predisposition may play a role in the pathogenesis of COME.