Presented at Association for Research in Otolaryngology Meeting, Phoenix, Arizona, U.S.A., February 6–10, 2008.
Article first published online: 13 JAN 2011
Copyright © 2011 The American Laryngological, Rhinological, and Otological Society, Inc.
Volume 121, Issue 2, pages 365–371, February 2011
How to Cite
MacArthur, C. J., Pillers, D.-A. M., Pang, J., Kempton, J. B. and Trune, D. R. (2011), Altered expression of middle and inner ear cytokines in mouse otitis media. The Laryngoscope, 121: 365–371. doi: 10.1002/lary.21349
Supported by NIH NIDCD R01 DC 09455 and NIDCD P30 DC005983. The authors have no other funding, financial relationships, or conflicts of interest to disclose.
- Issue published online: 26 JAN 2011
- Article first published online: 13 JAN 2011
- Manuscript Accepted: 1 SEP 2010
- Manuscript Revised: 31 AUG 2010
- Manuscript Received: 28 JUN 2010
- NIH NIDCD. Grant Number: R01 DC 09455
- NIDCD. Grant Number: P30 DC005983
- acute otitis media;
- chronic otitis media;
- middle ear;
- inner ear
The inner ear is at risk for sensorineural hearing loss in both acute and chronic otitis media (OM), but the mechanisms underlying sensorineural hearing loss are unknown. Previous gene expression array studies have shown that cytokine genes might be upregulated in the cochleas of mice with acute and chronic OM. This finding implies that the inner ear could manifest a direct inflammatory response to OM that may cause sensorineural damage. Therefore, to better understand inner ear cytokine gene expression during OM, quantitative real-time polymerase chain reaction and immunohistochemistry were used in mouse models to evaluate middle and inner ear inflammatory and remodeling cytokines.
Basic science experiment.
An acute OM model was created in Balb/c mice by a transtympanic injection of Streptococcuspneumoniae in one ear; the other ear was used as a control. C3H/HeJ mice were screened for unilateral chronic OM, with the noninfected ear serving as a control.
Both acute and chronic OM caused both the middle ear and inner tissues in these two mouse models to overexpress numerous cytokine genes related to tissue remodeling (tumor necrosis factor-α, bone morphogenetic proteins, fibroblast growth factors) and angiogenesis (vascular endothelial growth factor), as well as inflammatory cell proliferation (interleukin [IL]-1α,β, IL-2, IL-6). Immunohistochemistry confirmed that both the middle ear and inner ear tissues expressed these cytokines.
Cochlear tissues are capable of expressing cytokine mRNA that contributes to the inflammation and remodeling that occur in association with middle ear disease. This provides a potential molecular basis for the transient and permanent sensorineural hearing loss often reported with acute and chronic OM.