1996 Fiscal Year Final Research Report Summary
Effects of parasites on the gene expression of nitric oxide synthase and chemokine in macrophages
| Project/Area Number |
06670257
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
寄生虫学(含医用動物学)
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| Research Institution | TOTTORI UNIVERSITY |
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Principal Investigator |
FUKUMOTO Soji Tottori University, Department of Medical Zoology, Associate Professor, 医学部, 助教授 (60111126)
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| Co-Investigator(Kenkyū-buntansha) |
HIRAI Kazumitsu Tottori University, Department of Medical Zoology, Professor, 医学部, 教授 (20093940)
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| Project Period (FY) |
1994 – 1996
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| Keywords | parasite / macrophage / nitric oxide synthase / chemokine / gene expression / northern blot / Spirometra erimacei |
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| Research Abstract |
Nitric oxide (NO) is important in the ability of mouse macrophages to kill infectious organisms including parasites. An inducible form of NO synthase (iNOS) is responsible for high output generation of NO by macrophages after stimulation with cytokines and/or LPS.Chemoattactant peptides termed chemokine are important components of the inflammatory response. Alive plerocercoids of Spirometra erinacei suppressed the mRNA expression of iNOS and JE,murine homologue of monocyte chemotactic protein-1, and nitrite production of macrophages stimulated with IFN-gamma and LPS in vitro. Excretory/secretory (ES) products from plerocercoids also suppressed the induced iNOS and JE mRNA and reduce nitrite production in a dose dependent manner. The suppression of iNOS mRNA levels in macrophages cultured for 24 h with ES products varied with the nature of the stimuli ; IFN gamma/LPS-induced iNOS mRNA levels were effected less than were iNOS mRNA levels induced by IFNgamma/IL-2 or IFNgamma/TNFalpha. Similar findings were obtained when nitrite production was measured. Thus mRNA levels appear to be the primary target of ES products. The expression of the glyceraldehyde-3-phosphate dehydrogenase gene was unaffected by the ES products. The NO donor drugs, S-nitroso-acetyl-penicillamine or diethylamine dinitric oxide, were unable to kill plerocercoids in vitro in the absence of macrophages, therefore NO might not be important in the host's defense mechanism to plerocercoids. It is supposed that a main physiological role of this inhibitory factor in ES products might be selectively down regulation of LPS-inducible gene expressions such as chemokines (JE and gro-alpha/KC) thereby preventing the accumlation of leukocytes, but not preventing the iNOS expression specifically.
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