13
Views
20
CrossRef citations to date
0
Altmetric
Original Article

Interleukin-1α, Interleukin-1β and Interleukin-8 Gene Expression in Human Aural Cholesteatomas

, , &
Pages 302-306 | Published online: 08 Jul 2009
 

Abstract

Presented in part at the 18th midwinter research meeting of Association for Research in Otolaryngology, February 5, 1995, Florida.

Bone destruction is a common characteristic feature of chronic otitis media, especially aural cholesteatoma. A number of immunohistochemical studies have suggested that interleukin-1 (IL-1) may be responsible for cholesteatomatous bone destruction. We designed this study to present the mRNA expression patterns of IL-1 α, IL-β, and IL-8, which can induce and activate the leukocyte, the major reservoir of potent proteolytic enzymes. Total RNAs were extracted from aural cholesteatomas, external auditory canal skin (EACS), postauricular skin (PAS), and granulation tissues and transcribed into cDNAs. cDNAs were amplified by using PCR technique with primers for IL-1 α, IL-1β, IL-8, and β-actin. Amplified products were hybridized with each internal probe and the relative density was measured. in granulation tissues, the relative density of IL-lα was greater than that of other tissues. the ratio of IL-1β and IL-8 of aural cholesteatoma was significantly higher than that of EACS and PAS. We suggest that both of IL-lα and IL-1β may play a role in the pathological changes, and that IL-8, which is mainly produced from cholesteatomatous epithelium, may have an important role in the pathological changes of cholesteatomas.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.