| Budget Amount *help |
¥14,700,000 (Direct Cost: ¥14,700,000)
Fiscal Year 2005: ¥4,300,000 (Direct Cost: ¥4,300,000)
Fiscal Year 2004: ¥5,000,000 (Direct Cost: ¥5,000,000)
Fiscal Year 2003: ¥5,400,000 (Direct Cost: ¥5,400,000)
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| Research Abstract |
This project has attempted to clarify the molecular mechanism and genetic background in the pathogenesis of chronic obstructive pulmonary disease (COPD) and bronchial asthma. It has been demonstrated that various inflammatory cells and mediators, and oxidative stresses are involved in the pathogenesis of these diseases. In addition, airway infection such as bacterial and viral infection play a role in the pathogenesis, progression and modification of these diseases. This project have shown that 1)a role of mitogen-activated protein kinase (MAPK) in airway inflammation via toll-like receptor(TLR)-2 and -4-dependent activation, 2)a role of oxidative stress-sensitive signaling molecule, ASK-1 in airway inflammation using ASK-1 knockout mice, 3)a role of endogenous anti-inflammatory molecules, A20, in airway inflammation in vitro and in vivo. In conclusion, for attenuating the airway inflammation seen in COPD and bronchial asthma, ASK-1 could be a molecular target for the therapy. Furtherm
… More
ore, A20 could be useful molecule to control the excessive inflammation. This project has attempted to clarify the molecular mechanism and genetic background in the pathogenesis of chronic obstructive pulmonary disease (COPD) and bronchial asthma. It has been demonstrated that various inflammatory cells and mediators, and oxidative stresses are involved in the pathogenesis of these diseases. In addition, airway infection such as bacterial and viral infection play a role in the pathogenesis, progression and modification of these diseases. This project have shown that 1)a role of mitogen-activated protein kinase (MAPK) in airway inflammation via toll-like receptor (TLR)-2 and -4-dependent activation, 2)a role of oxidative stress-sensitive signaling molecule, ASK-1 in airway inflammation using ASK-1 knockout mice, 3)a role of endogenous anti-inflammatory molecules, A20, in airway inflammation in vitro and in vivo. In conclusion, for attenuating the airway inflammation seen in COPD and bronchial asthma, ASK-1 could be a molecular target for the therapy. Furthermore, A20 could be useful molecule to control the excessive inflammation. Less
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