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Therapy and molecular mechanisms of middle ear mucosal proliferation caused by apoptosis during bacterial otitis media

Research Project

Project/Area Number 18591886
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Otorhinolaryngology
Research InstitutionJuntendo University

Principal Investigator

FNRUKAWA Masayuki  Juntendo University, Medical School, Assistant Professor (20359524)

Co-Investigator(Kenkyū-buntansha) IKEDA Katsuhisa  JUNTENDO UNIVERSITY, Medical School, Professor (70159614)
YOKOI Hidenori  JUNTENDO UNIVERSITY, Medical School, Assistant Professor (80317487)
Project Period (FY) 2006 – 2007
Project Status Completed (Fiscal Year 2007)
Budget Amount *help
¥3,790,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥390,000)
Fiscal Year 2007: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2006: ¥2,100,000 (Direct Cost: ¥2,100,000)
KeywordsJNK / mucosal hyperplasia / otitis media / 中耳粘膜肥厚 / TUNEL / caspase
Research Abstract

Mucosal hyperplasia is a characteristic component of otitis media. The present study investigated the participation of signaling via the Jun N-terminal protein kinase (JNK) mitogen-activated protein kinase in middle ear mucosal hyperplasia in animal models of bacterial otitis media. Otitis media was induced by the inoculation of nontypeable Haemophilus influenzae into the middle ear cavity. Western blotting revealed that phosphorylation of JNK isoforms in the middle ear mucosa preceded but paralleled mucosal hyperplasia in this in vivo rat model. Nuclear JNK phosphorylation was observed in many cells of both the mucosal epithelium and stroma by immunohistochemistry. In an in vitro model of primary rat middle ear mucosal explants, bacterially induced mucosal growth was blocked by the Rac/Cdc42 inhibitor Clostridium difficile toxin B, the mixed-lineage kinase inhibitor CEP11004, and the JNK inhibitor SP600125. Finally, the JNK inhibitor SP600125 significantly inhibited mucosal hyperplasia during in vivo bacterial otitis media in guinea pigs. Inhibition of JNK in vivo resulted in a diminished proliferative response, as shown by a local decrease in proliferating cell nuclear antigen protein expression by immunohistochemistry. We conclude that activation of JNK is a critical pathway for bacterially induced mucosal hyperplasia during otitis media, influencing tissue proliferation.

Report

(3 results)
  • 2007 Annual Research Report   Final Research Report Summary
  • 2006 Annual Research Report
  • Research Products

    (3 results)

All 2007

All Journal Article (3 results) (of which Peer Reviewed: 2 results)

  • [Journal Article] Jun N-terminal protein kinase enhances middle ear mucosal proliferation during bacterial otitis media.2007

    • Author(s)
      Furukawa M, Ebmeyer J, Pak K, Austin DA, Melhus A, Webster NJ, Ryan AF.
    • Journal Title

      Infection and Immunity. 75

      Pages: 2562-2571

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2007 Final Research Report Summary
    • Peer Reviewed
  • [Journal Article] Webster NJ, Eyan AF. Jun N-terminal protein kinase Jun Nterminal protein kinase enhances middle ear mucosal proliferation during bacterial otitis media.2007

    • Author(s)
      Furukawa M, Ebmeyer J, Pak K, Austin DA, Melhus A
    • Journal Title

      Infection and Immunity 75

      Pages: 2562-2571

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2007 Final Research Report Summary
  • [Journal Article] Jun N-terminal protein kinase enhances middle ear mucosal proliferation during bacterial otitis media2007

    • Author(s)
      Furukawa M, Ebmeyer J, Pak K, Austin DA, Melhus A, Webster NJ, Ryan AF
    • Journal Title

      Infection&Immunity 75

      Pages: 2562-2571

    • Related Report
      2007 Annual Research Report
    • Peer Reviewed

URL: 

Published: 2006-04-01   Modified: 2016-04-21  

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