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Murine Model of Interleukin‐8‐Induced Otitis Media
Author(s) -
Johnson Michael,
Leonard Gerald,
Kreutzer Donald L.
Publication year - 1997
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 - 10.1097/00005537-199710000-00020
Subject(s) - middle ear , otitis , inflammation , medicine , saline , interleukin , infiltration (hvac) , pathology , immunology , anatomy , cytokine , endocrinology , surgery , physics , thermodynamics
Interleukin‐8 (IL‐8), a potent inflammatory mediator that is thought to control leukocyte recruitment and activation during inflammatory reactions, has been implicated in a variety of inflammatory diseases. Recent studies in our laboratory have demonstrated the presence of IL‐8 in chronically inflamed human middle ear effusions. These data have led us to hypothesize that IL‐8 is responsible for the leukocyte recruitment seen in otitis media. Because the effect of IL‐8 on the middle ear mucosa has not been investigated and therefore its role in middle ear inflammation is not known, we investigated the ability of IL‐8 to directly induce inflammation in the murine middle ear. For these studies, ICR mice were used to test the hypothesis that IL‐8 could directly induce inflammation in the middle ear. Murine middle ears received 8‐mL transtympanic injections of human IL‐8 (25 mg/mL) in saline, heat‐killed Streptococcus pneumoniae (1 × 10 8 /mL), or normal saline. Temporal bones were removed at 1, 4, 8, 24, and 48 hours, decalcified, and processed for histologic examination. Noninjected murine temporal bones served as controls. Normal saline‐injected ears demonstrated little to no change as compared with temporal bones from noninjected ears. IL‐8‐injected ears histologically demonstrated thickening of the epithelial layer and subepithelial space (SES), with inflammatory cell infiltration in the SES peaking at 4 to 8 hours and resolving by 48 hours. Bacteria‐injected ears demonstrated findings similar to, although not as extensive as, those found in IL‐8‐injected ears (i.e., inflammatory reactions peaked at 8 to 24 hours and resolved by 72 hours). Our results demonstrate that IL‐8 is a potent inducer of middle ear inflammation and support the concept that IL‐8 may be one of the key cytokines responsible for the leukocyte accumulation and activation seen in otitis media.