| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Outline of Final Research Achievements |
Infections mainly caused exacerbations in chronic obstructive pulmonary disease (COPD). However, the mechanisms in which COPD exacerbations occur remain to be elucidated. We hypothesized that the capacities to recognize bacteria including pseudomonous and streptococcus pneumonia by NODs1 and 2, some of pattern recognition molecules, are intact and still the downstream pathway of NODs for innate immunity including autophagy pathway (ATG16L1 and other autophagy proteins are involved) fail to function in frequent-exacerbators. The expression level of the cytokine IL10 was higher in the monocytes derived from COPD subjects with ATG16L1 300Ala genotype, which was related to frequent exacerbators. A single nucleotide polymorphism rs2075820 in NOD1 was associated with airflow limitation in COPD and NOD1 stimulant was related to the activation of p38 pathway in vitro. Thus, bacterial colonization is thought to promote airflow limitation by NOD1 stimulation and the activation of p38 pathway.
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