| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2012: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2011: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2010: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Research Abstract |
Although there is little clinical evidence about whether or not lung injury practically occurs in fetuses with chorioamnionitis, this possibly means that some of the infants with BPD had already suffered parenchymal lung injury while in utero. We have previously shown that, in most of moderate/severe BPD infants, the plasma KL-6 level was already increased in the cord blood plasma, especially when the infants were exposed to chorioamnionitis. Therefore, it seems likely that prenatal lung injury associated with chorioamnionitis usually has a priming effect that predisposes fetal lungs to become more susceptible to subsequent toxic agents, rather than lung injury being directly induced by intrauterine infection. Recently, it is gradually known that the redox environment surrounding cells / tissues possibly influence the cellular viability such as growth, differentiation, or apoptosis. We hypothesized that the redox environment of pulmonary epithelial lining fluids may be collapsed when the infants were exposed to placental infections, and may lead to the development of severe BPD because of impaired growth / differentiation of their lungs. We measured the oxidized to reduced ratio of major small-molecular antioxidants in pulmonary epithelial lining fluids such as ascorbic acid, glutathione, and uric acid in the preterm infants born before 28 week gestation. As a result, both of the ratios of dehydroascorbic acid / reduced ascorbic acid and glutathione disulfide / reduced glutathione were increased in the infants with placental infections subsequently developed BPD. Especially, dehydroascorbic acid / reduced ascorbic acid ratio was in good correlation with the values of IgM and KL-6 in cord blood plasma. Therefore, it was clearly shown that the redox environment of pulmonary epithelial lining fluids was dysregulated in the infants with placental infection.
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