1995 Fiscal Year Final Research Report Summary
Th1/Th2 cytokine responses of Angiostrongyluscantonensis infected mice
| Project/Area Number |
06670251
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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 |
寄生虫学(含医用動物学)
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| Research Institution | AKITA UNIVERSITY |
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Principal Investigator |
YOSHIMURA Kentaro Akita University, School of Medicine, Professor, 医学部, 教授 (90053058)
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| Co-Investigator(Kenkyū-buntansha) |
SHIMADA Hiroko (SUGAYA Hi) Akita University, School of Medicine, Research, 医学部, 助手 (30235626)
ISHIDA Kazuto Akita University, School of Medicine, Research Associate, 医学部, 助手 (60006731)
ABE Tatsuya Akita University, School of Medicine, Associate Professor, 医学部, 助教授 (80128363)
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| Project Period (FY) |
1994 – 1995
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| Keywords | Angiostrongylus cantonensis / Mesocestoides corti / eosinophil / Th1 cytokine / Th2 cytokine / RT-PCR / IL-5 transgenic mice / IL-5 receptor alpha knockout mice |
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| Research Abstract |
This study yielded the following results : 1. When BALB/cand C57BL/6, susceptible and resistant strains respectively, were infected with Angiostrongylus cantonensis, they developed IL-5 cytokine responses in their cerebrospinal fluid (CSF) with a peak response at days 12-15 postinfection (p.i.), suggesting this being the major cause of CSF eosinophilia. 2. T cells in CSF showed IL-5, IL-4, and IL-2 mRNA expressions but not IFN-gamma mRNA.3. There was no significant differencein production of the 4 kinds of cytokines between two mouse strains. 4. When BALB/c mice were previously infected with Mesocestoides corti 7-18 days prior to A.cantonensis infection, these mice showed mild morbidity and low mortality as compared with mice with monoinfection with A.cantonensis. This might be caused by the low worm recovery in the mice concurrently infected with M.corti and A.can tonensis at around 30 days p.i. 5. M.corti infected mice developed Th2 dominant cytokine responses and also showed a signi
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ficantly higher IL-2 response than A.cantonensis infected mice. 6. Mild morbidity and low mortality observed in BALB/c mice concurrentlyinfected with M.corti and A.cantonensis can not be explained by the above 4 kinds of cytokine responses. 7. IL-5 transgenic mice infected with A.cantonensis killed the intracranial worms more rapidly than C3H/HeN control mice. These infected IL-5 transgenic mice showed much higher CSF eosinophilia than C3H/HeN mice. 8. Prominent eosinophil infiltration was noted around the blood vessels in the meninges of A.cantonensis infected IL-5 transgenic mice and also around the worms parasitizing in their subarachnoid spaces. Most of these eosinophils were found degranulated. 9. IL-5 receptor alpha gene knockout mice infected with A.cantonensis showed a significantly higher intracranial worm recovery than infected heterozygous or wild-type mice. Contrarily, the infected IL-5 receptor knockout mice showed extremely low CSF eosinophilia. These data clearly indicate that A.cantonensis infected mice induce Th2 dominant cytokine responses, especially IL-5, in the local CSF,which in turn evoke prominent CSF eosinophilia. CSF eosinophils are then involved in the killing of intracranial worms. Less
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