KAWASAKI Yukihiko Fukushima Medical University School of Medicine, Pediatrics, Research Associate, 医学部, 助手 (00305369)
SUZUKI Junzo Fukushima Medical University School of Medicine, Pediatrics, Associate Professor, 医学部, 助教授 (20171217)
SUZUKI Hitoshi Fukushima Medical University School of Medicine, Pediatrics, Professor, 医学部, 教授 (80045682)
|Budget Amount *help
¥1,300,000 (Direct Cost : ¥1,300,000)
Fiscal Year 2000 : ¥500,000 (Direct Cost : ¥500,000)
Fiscal Year 1999 : ¥800,000 (Direct Cost : ¥800,000)
The etiology or aggravation factors of glomerulonephritis, such as IgA nephropathy, is still unclear. Episodes of nephritis are frequently proceeded by acute viral infections, therefore, we examined how viral infection would be participating in the exacerbation of anti-GBM nephritis in mice.
Male BALB/c mice were injected intravenously with a single dose of anti-GBM antibody. Coxsackievirus B4 (CoxB4), in the group of enterovirus and minimum RNA virus, was inoculated intravenously into the nephritis induced mice. These mice were divided into three groups ; in group A, CoxB4 was injected intravenously on day 0, simultaneously with anti-GBM antibody injection, : in group B, CoxB4 was injected intravenously on day 7, when urinary findings worsening, : in group C (control group), anti-GBM antibody was alone injected, no challenged with virus. The amount of urine protein excretion and various cytokines were measured with time. Moreover, these mice were sacrificed, and the kidneys were collected for light microscopy, immunohistochemistory, and measurements of the message levels of various cytokines from 2 to 14 days.
The amounts of urinary protein excretion were significantly increased in group A, than group B or group C.
These results indicate that the course of nephritis in mice was influenced by viral infections, especially on early stage infections.