| Project/Area Number |
63570293
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
内科学一般
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| Research Institution | Tokushima University School of Medicine |
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Principal Investigator |
SONE Saburo Tokushima Univ. Sch. of Med., Lecturer, 医学部・附属病院, 講師 (40145024)
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| Co-Investigator(Kenkyū-buntansha) |
OKUBO Akio Tokushima University School of Medicine Assistant internist, 医学部・附属病院, 助手 (90203728)
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| Project Period (FY) |
1988 – 1989
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| Project Status |
Completed (Fiscal Year 1989)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1989: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1988: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | Monocyte / Alveolar macrophage / Monokine / Interleukin 1 / Lung cancer / tumor necrosis factor / モノカイン / マクロファージ モノカイン / インターロイキン1 / 腫瘍壊死因子 / 肺癌 / リポソーム / 細胞障害作用 |
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| Research Abstract |
The present studies were performed to elucidate the mechaniss by which human activated mosocyte-macrophages kill tumor cells. Membrane-associated interieukin 1alpha (IL-1alpha ) induced by synergistic actions of IFN-gamma and synthetic adjutant, was found to be a mediator of human monodyte-mediated tumor cell killing. Human alveolar macrophages and monocyte-derived macrophages had abilities to produce cell-associated IL-1alpa activity and tamior necrosis factor (TNF) more than blood sonocytes. We also found that human monocyte-mediated cytotoxicity against human selanona (A375) cells was mediated in part by a new tumor cytotoxic factor (KW, 30,000; PI 6), differing from IL-1 and TMF-alpha. Abilities of blood monocytes of lung cancer patients to express antitamor activity and to produce IL-1 were analyzed. The presence of lung cancer significantly increased the number of barvested blood monocytes. Spontaneous tumoricidel activity of these monocutes was slightly high as compared to those of healthy donors. Nevertheless, there was no difference in production of IL-1 between two groups. Blood monocutes of lung cancer patients were less cytotaxic than healthy donors subsequent to incubation with synthetic immunoadjuvant, but were as tomoricidal as those from healthy donors when activated with liposome-entrapped immunoadjuvant. Human II-2-activated killer cells were cytotoxic to alveolar macrophages and to macrophates matured by GM-CSF from blood sonocytes. These observations suggest that alveolar macrophages may play a critical role in situ regulation of pulmonary inflammatory and immune reactions through production of cell- associated IL-1alpha and INF.
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