Association of microRNA 146 with middle ear hyperplasia in pediatric otitis media

详细信息    查看全文

• 作者：Tina L. Samuels^a ; Justin Yan^a ; Pawjai Khampang^a ; Alexander MacKinnon^b ; Wenzhou Hong^a ; Nikki Johnston^a ; ^c ; Joseph E. Kerschner^a ; ^{jkerschner@mcw.edu" class="auth_mail" title="E-mail the corresponding author}
• 关键词：Otitis media ; miR-146a ; miR-146b ; IRAK1 ; TRAF6 ; Toll-like receptor
• 刊名：International Journal of Pediatric Otorhinolaryngology
• 出版年：2016
• 出版时间：September 2016
• 年：2016
• 卷：88
• 期：Complete
• 页码：104-108
• 全文大小：757 K

文摘

Toll-like receptor signaling activated by bacterial otitis media pathogens in the middle ear has been shown to play a key role in OM susceptibility, pathogenesis and recovery. Recent studies implicate microRNA 146 (miR-146) in regulation of inflammation via negative feedback of toll-like receptor signaling (TLR) in a wide variety of tissues, however its involvement in otitis media is unknown.

Methods

Human middle ear epithelial cells were stimulated with proinflammatory cytokines, interleukin 1 beta or tumor necrosis factor alpha, for two to twenty-four hours. Middle ear biopsies were collected from children with otitis media with effusion (n = 20), recurrent otitis media (n = 9), and control subjects undergoing cochlear implantation (n = 10). miR-146a, miR-146b expression was assayed by quantitative PCR (qPCR). Expression of miR-146 targets involved in TLR signaling, IRAK1 and TRAF6, was assayed by qPCR in middle ear biopsies. Middle ear biopsies were cryosectioned and epithelial thickness measured by a certified pathologist.

Results

Proinflammatory cytokines induced expression of miR-146 in middle ear epithelial cells in vitro. Middle ear miR-146a and miR-146b expression was elevated in otitis media patients relative to control subjects and correlated with middle ear epithelial thickness. A trend towards inverse correlation was observed between miR-146 and TRAF6 expression in the clinical population.

Conclusions

This report is the first to assess miRNA expression in a clinical population with OM. Findings herein suggest miR-146 may play a role in OM.