1995 Fiscal Year Final Research Report Summary
ROLE OF ALVEOLAR MACROPHAGES IN PATHOGENESIS OF PULMONARY EMPHYSEMA
| Project/Area Number |
05404031
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| Research Category |
Grant-in-Aid for General Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | HOKKAIDO UNIVERSITY |
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Principal Investigator |
KAWAKAMI Yoshikazu HOKKAIDO UNIVERSITY SCHOOL OF MEDICINE PROFESSOR, 医学部, 教授 (10001877)
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| Co-Investigator(Kenkyū-buntansha) |
NISHIMURA Masaharu HOKKAIDO UNIVERSITY HOSPITAL LECTURER, 医学部附属病院, 講師 (00208224)
MIYAMOTO Kenji HOKKAIDO UNIVERSITY SCHOOL OF MEDICINE ASSOCIATE PROFESSOR, 医学部, 助教授 (50190814)
KONDO Takahito NAGASAKI UNIVERSITY SCHOOL OF MEDICINE PROFESSOR, 医学部, 教授 (00158908)
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| Project Period (FY) |
1993 – 1995
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| Keywords | Emphysema / Computed tomography / Bronchoalveolar lavage / Alveolar macrophage / Neutrophil elastase / Oxidant / Antioxidant / Elastin |
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| Research Abstract |
Alveolar macrophages (AMs) are thought to be involved in the development of pulmonary emphysems. We focused on neutrophil elastase (NE) associated with AMs. The purpose of this study was to elucidate the activity and releasability of NE in AMs, and to examine its possible relationship with the development of pulmonary emphysema. Thirty-six older smokers and nonsmorkers, who were all community volunteers, were evaluated for the presence of emphysematous changes on CT scans. Bronchoalveolar lavage (BAL) was performed to obtain AMs from all the subjects. Esterolytic activity using an NE-sensitive substrate (MEOSAAPVNA) was elevated in AMs from current smorkers with emphysematous changes on CT scans compared to those from current smorkers without emphysematous changes (p<0.05). We also demonstrated the accelerated releasability of NE from AMs in the subjects with emphysematous changes.
To evaluate the linkage of elastases with development of pulmonary emphysema, we measured NE and Cathepsin B,L in BAL fluid from 39 older volunteers by ELISA and also elastin-degrated peptides (EDP) as a biochemical marker of excessive elastin degradation. NE was significantly elevated in smokers with emphysematous changes compared not only with nonsmokers (p<0.01), but also with current smokers without emphysematous changes (p<0.01). Cathepsin B and L were not related with smoking status or presence of emphysematous changes on CT scans. The concentration of EDP in BAL fluid was significantly higher in current smokers than noncurrent smokers (p<0.01) and was significantly related with NE-alpha1-proteinase inhibitor complex in BAL fluid (r=0.38, p<0.05).
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