| Project/Area Number |
24591150
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Tohoku University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
NARA Masayuki 東北大学, 病院, 特任教授 (70374999)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 気道分泌 / パッチクランプ / Toll様受容体 / 粘膜免疫 / Flagellin / Nitric oxide / 気道粘膜下腺 / COPD増悪 / 難治性喘息 / LPS / アセチルコリン / 電解質分泌 / 一酸化窒素 |
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| Outline of Final Research Achievements |
The direct relationship between Toll like receptors (TLRs) and airway serous secretion has not been well investigated. Here, we focused on whether TLR5 ligand flagellin, which is one of the components of Pseudomonas aeruginosa, is involved in the upregulation of airway serous secretion. We revealed a novel potentiating effect of Flagellin/TLR5 signaling in airway serous secretion that was independent of LPS/TLR4 signaling. These findings suggest that TLR5 takes part in the airway mucosaldefense systems as a unique endogenous potentiator of airway serous secretions and that NO/cGMP/cGK signaling is involved in this rapid potentiation by TLR5 signaling. Thus, it is suggested that pathogens with these TLRs-ligands are able to cause hypersecretion in the airway even in cases of colonization. We believe that these findings could offer a new therapeutic candidate for controlling airway secretion in chronic inflammatory airway diseases, such as COPD and severe asthma.
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