1994 Fiscal Year Final Research Report Summary
STUDIES ON THE PATHOGENESIS OF PIE SYNDROME INDUCED BY NEMATODE INFECTION,WITH SPECIAL REFERENCE TO THE ROLE OF MAST CELLS.
Project/Area Number |
05670235
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Research Category |
Grant-in-Aid for General Scientific Research (C)
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Allocation Type | Single-year Grants |
Research Field |
寄生虫学(含医用動物学)
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Research Institution | KYOTO PREFECTURAL UNIVERSITY OF MEDICINE |
Principal Investigator |
ARIZONO Naoki KYOTO PREFECTURAL UNIVERSITY OF MEDICINE,DEPARTMENT OF MEDICAL ZOOLOGY,PROFESSOR, 医学部, 教授 (10079725)
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Co-Investigator(Kenkyū-buntansha) |
TEGOSHI Tatsuya KYOTO PREFECTURAL UNIVERSITY OF MEDICINE,DEPARTMENT OF MEDICAL ZOOLOGY,RESEARCH, 医学部, 助手 (40254370)
YAMADA Minoru KYOTO PREFECTURAL UNIVERSITY OF MEDICINE,DEPARTMENT OF MEDICAL ZOOLOGY,LECTURER, 医学部, 講師 (70106392)
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Project Period (FY) |
1993 – 1994
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Keywords | PIE syndrome / Loeffler's syndrome / Mast cell / Nematode / Nippostrongylus / Eosinophil / Ws / Ws rat |
Research Abstract |
Infection with the nematode Nippostrongylus brasiliensis induces tissue eosinophilia, increases of the number of mast cells, and development of granulomas in rat lung after the migration of larvae through this organ. This lung lesion resembled Loeffler's syndrome, that is one of PIE syndrome. To know the role of mast cells in the development of lung lesion, we investigated the nematode-induced tissue eosinophilia and granuloma formation in congenitally mast cell-deficient Ws/Ws rats. Numbers of the worms in the lung and the time course of migration through the lung did not differ between Ws/Ws and control +/+ rats. Eosinophils increased 1-7 days after primary as well as after the challenge infection. The numbers of eosinophils in the lung tissue and in bronchoalveolar lavage fluid were significantly smaller in Ws/Ws rats than in +/+ rats. In +/+ rats, granulomas developed 7 days after the primary infection. The granulomas consists of epithelioid cells, multinucleate giant cells, eosinophils and mast cells. After challenge infection on day 28, granulomas developed more quickly, peaked 3 days after the challenge infection, and the granuloma size was significantly larger than that in primary infection. Compared to +/+ rats, the granuloma formation, especially that after the challenge infection, was significantly suppressed in Ws/Ws rats. In +/+ rats, the number of mast cells markedly increased after the primary infection. After the challenge infection, the numbers decreased transiently 1-3 days later, suggesting that mast cells were activated and invisualized. This was supported by the observations that the levels of histamine and rat mast cell protease II in the lung tissue extract were decreased at this period. These results indicate that mast cells play an important role for the development of granuloma and tissue eosinophilia in the lung.
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