2006 Fiscal Year Final Research Report Summary
Exploring molecular pathogenesis related to inflammatory cytokines in protracted otitis media.
Project/Area Number |
17591783
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Otorhinolaryngology
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Research Institution | Hamamatsu University School of Medicine |
Principal Investigator |
WATANABE Takahiro Hamamatsu University School of Medicine, Otolaryngology, Senior Assistant Professor (90303552)
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Co-Investigator(Kenkyū-buntansha) |
IWAKAKI Satoshi Hamamatsu University School of Medicine, Otolaryngology, Senior Assistant Professor (00232653)
NAGURA Mitsuyoshi Hamamatsu University School of Medicine, Otolaryngology, Senior Assistant Professor (50334983)
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Project Period (FY) |
2005 – 2006
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Keywords | inflammatory cytokine / otitis media / lipopolysaccharide / NF-κB |
Research Abstract |
Bacterial infection in the middle ear causes synthesis of inflammatory cytokines and chemokine. It is believed overproduction of cytokines play a critical role in pathogenesis of protracted otitis media. Bacterial components, such as LPS, accumulated in the middle ear may continue to induce inflammatory response. Human epithelial cell lines were used in the project. Epithelial cells, which are exposed to pathogen components derived from Nontypeable Haemophilus influenzae (NTHi) and LPS, demonstrate activation of NF-κB. The studies using proteasome inhibitor and p38 MAPK inhibitor showed both IKK-IkBα and p38 MAPK pathways are required in NF-κB activation caused by bacterial infection. In conclusion, our studies demonstrate inflammatory response caused by NTHi infection requires both IKK-IκBα and p38 MAPK pathways. Two pathways are also implicated in regulating inflammatory cytokines and chemokine, such as TNF-α, IL-lβ, and IL-8. Our future studies will focus on investigating synthesis of cell adhesion molecules required for the infiltration of inflammatory cells. Our future studies will focus on investigating synthesis of cell adhesion molecules required for the infiltration of inflammatory cells.
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