1996 Fiscal Year Final Research Report Summary
Immuno-pathological studies in IgA nephropathy : The role of virus for etiological and progressive factors
| Project/Area Number |
06670813
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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 |
Pediatrics
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| Research Institution | Fukushima Medical College |
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Principal Investigator |
SUZUKI Hitoshi Fukushima Medical College, Pediatrics Professor, 医学部, 教授 (80045682)
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| Co-Investigator(Kenkyū-buntansha) |
SUZUKI Shigeo Fukushima Medical College, Pediatrics Reseach Associate, 医学部, 助手 (00274960)
KUME Kazunari Fukushima Medical College, Pediatrics Assistant Professor, 医学部, 講師 (40254023)
SUZUKI Junzo Fukushima Medical College, Pediatrics Associate Professor, 医学部, 助教授 (20171217)
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| Project Period (FY) |
1994 – 1996
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| Keywords | Experimental IgA nephropathy / Coxsackie B_4 virus / In situ hybridization / in situ hybridization法 |
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| Research Abstract |
Viruses have been suspected to be etiological agents of IgA nephropathy. Recently, viruses were detected in renal tissues from patients with IgA nephropathy. We tried to cause lesions similar to IgA nephropathy by inoculating virus into mice and to detect virus RNA in the lesion by in situ hybridization. A group of mice were inoculated intravenously with coxsackie B_4 virus once a month from 1 to 5 months of age and sacrificed monthly from 6 to 12 months of age. Mesangial proliferation and deposits that stained positive with periodic acid-Schiff in light microscopy and electron-dense deposits in electron microscopy were found from 6 months of age. Positive findings for IgG and IgA deposition in the mesangium were noted and the intensity of IgA deposition was predominant after 10 months of age. The signals of coxsackie B_4 virus by in situ hybridization were observed in the lesions. These observations indicate that coxsackie B_4 virus inoculated repeatedly into mice induces lesions similar to IgA nephropathy. The depositions of the lesions may be immune complexes of coxsackie B_4 virus and these immune complexes injure renal tissues.
Lesions very similar to human IgA nephropathy could be caused in mice by repeated infections of well-known virus. If further studies demonstrate an early from of glomerular lesions and a predominant deposition for IgA,our experimental model may be useful to clarify the mechanism of human IgA nephropathy.
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Research Products
(2 results)
