2003 Fiscal Year Final Research Report Summary
Immuno-pathological studies in IgA nephropathy : The role of virus for etiological and progressive factors
| Project/Area Number |
13670823
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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 University School of Medicine Grant-in-Aid for Scientific Research (C) (2) |
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Principal Investigator |
SUZUKI Hitoshi Fukushima Medical University School of Medicine, Pediatrics Professor, 医学部, 教授 (80045682)
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| Co-Investigator(Kenkyū-buntansha) |
YUKIHIKO Kawasaki Fukushima Medical University School of Medicine, Research Associate, 医学部, 助手 (00305369)
HOSOYA Mitsuaki Fukushima Medical University School of Medicine, Assistant Professor, 医学部, 講師 (80192318)
SUZUKI Junzo Fukushima Medical University School of Medicine, Associate Professor, 医学部, 助教授 (20171217)
ISOME Masato Fukushima Medical University School of Medicine, Research Associate, 医学部, 助手 (00363747)
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| Project Period (FY) |
2001 – 2003
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| Keywords | IgA nephropathy / Coxsackievirus / Higa mice |
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| Research Abstract |
IgA nephropathy is an idiopathic glomerulonephritis characterized by predominant IgA deposition. IgA nephropathy is the most common form of glomerulonephritis in the world. However, the etiology of this disease is still unclear. In IgA nephropathy renal symptoms are frequently preceded by episodes of upper respiratory tract infections and/or gastrointestinal infections, suggesting viruses as the etiology of this disease.
There have been some reports on human nephritis and experimental models associated with acute viral infection, including coxsackie viruses. We previously reported that IgG and IgA were stained in a mesangial pattern in glomeruli after mice were inoculated intravenously with Cox. B4 virus monthly for 9 months although IgA deposits were not dominant.
Therefore, we examined coxsackie virus and adenovirus receptor (CAR), has been identified as a common cellular receptor for both viruses, expression and localization in rat glomeruli using puromycin aminonucleoside (PAN) nephrosis and found that a significant increase in CAR staining intensity along the glomerular capillary wall in PAN nephrosis. These results suggest that coxsackie viruses directly infects in podocytes of glomeruli.
And, we evaluated the efficacy of coxsackie viruses B4 for experimental models and. found that coxsackie B4 virus inoculated repeatedly into mice induces the increase of urinary protein excretion and the mesangial proliferation in anti-GBM nephritis. These findings suggest that coxsackie viruses B4 make the pathological condition of chronic glomerulonephritis worse.
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