| Co-Investigator(Kenkyū-buntansha) |
ITAKURA Yukino Medical School, Assitant, 医学部, 助手 (70223071)
TAKASAKI Jiro Medical School, Assitant Professor, 医学部, 講師 (30197082)
SHIMIZU Hiroshi Medical School, Associate Professor, 医学部, 助教授 (90260843)
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| Research Abstract |
The incidence of chronic lung disease (CLD) reaches 20% of the very low birth weight infants. In the present study, we tried to understand the pathogenesis of CLD and develop strategy for prevention and treatment of CLD.
1)Subfractions of pulmonary surfactant under high frequency oscillatory ventilation
We made a rabbit model of acute respiratory distress syndrome, then performed conventional mandatory ventilation (CMV) or high frequency oscillatory ventilation (HFOV). After 4h ventilation, bronchoalveolar lavage fluid was collected. Surfactant subtype was fractionated using ultracentrifugation and surfactant subtype conversion was evaluated in each ventilatory mode. We could demonstrate that HFOV was superior to CMV in terms of surfactant subtype conversion.
2)Congenital alveolar proteinosis and surfactant protein B deficiency in Japan
Congenital alveolar proteinosis (CAP) is classified into type VI CLD. Two cases of CAP and one case of partial surfactant protein B(SP-B) deficiency were identified in Japan between 1998 and 2002. Typical SP-B deficiency with a frame shift mutation, 121ins2, leading to a truncated nonfunctional SP-B, was not identified. We also analyzed abundance of the deletion form of SP-B mRNA, i.e., alternatively spliced SP-B mRNA in 3 cases of CAP. The contents of the "minor" SP-B mRNA in those patients were higher as compared to those in normal lungs.
3)Anti-IL-8 autoantibody in the tracheobronchial aspirates in infants with CLD
We reported previously a large amount of IL-8 in tracheobronchial aspirates during the early stage of life in type III CLD. In the present study, anti-IL-8 IgM antibody in infants with type III CLD was significantly higher as compared to type I, type II, and type V CLD. The presence of anti-IL-8 autoantibody seems to be the mechanism that limits the bioavailability of free IL-8 in the lung.
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