| Budget Amount *help |
¥4,010,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥510,000)
Fiscal Year 2007: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2006: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Research Abstract |
Acidification of airway systems has been reported to be associated with bronchial asthma and low pH could be contributed substantially to airway inflammation. To evaluate the mRNA expression of proton sensing G-protein-coupled receptors in human smooth muscle cells (SSMC) and bronchial epithelial cells, real-time PCR was performed. OGR1 was predominantly expressed in BSMC. Extracellular acidic pH induced IL -6 production and it was markedly inhibited by sIRNA specific OGR1. To investigate the role of OGR1 in chronic airway inflammation, especially bronchial asthma, a murine allergic asthma model sensitized with ovalbumin (OVA) was studied. We are comparing OGR1 knock-out BALB/c mice and wild mice in airway responsiveness to inhaled methacholine, inflammatory cells accumulation in bronchoalveolar lavage fluid (BALF), histology, anti-OVA IgE, and cytokines in BALF. On the other hand, we were interested in the effect of rsolvin E1, an anti-inflammatory lipid mediator, on airway inflammation. In a murine allergic asthma model, resolvin E1 inhibited eosinophil and lymphocyte recruitment, IL-13 in BALF, OVA specific IgE in serum as well as airway hyperfesposiveness to inhaled methacholine. Moreover, resolvin E1-treated mice had significantly lower mucus scores compared to vehicle-treated mice based on the number of goblet cells stained with PAS.
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