| Project/Area Number |
09671147
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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 |
Kidney internal medicine
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| Research Institution | Institute of Clinical Medicine, University of Tsukuba |
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Principal Investigator |
KOYAMA Akio Institute of Clinical Medicine, University of Tsukuba, 臨床医学系, 教授 (80111384)
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| Co-Investigator(Kenkyū-buntansha) |
室 かおり 筑波大学, 臨床医学系, 助手 (60301082)
KIKUCHI Shuichi Institute of Clinical Medicine, University of Tsukuba, 臨床医学系, 講師 (40282355)
平山 浩一 筑波大学, 臨床医学系, 講師 (10302423)
KOBAYASHI Masaki Institute of Basic Medical Sciences, University of Tsukuba
小林 正貴 東京医科大学, 霞ヶ浦病院, 講師 (10195810)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 1998: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 1997: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | superantigen / T cell receptor / post-MRSA glomerulonephritis / cytokine / systemic vasculitis / superantigen-related nephritis / 全身性血管炎 / スーパー抗原関連腎炎 / ネフローゼ症候群 / メチシリン耐性ブドウ球菌 / 血管炎 / エンテロトキシン |
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| Research Abstract |
Background. We have previously reported that 10 patients who developed glomerulonephritis (GN) in association with methicillin-resistant staphylococcus aureus (MRSA) infection showed a marked increase in T cells both in DR+CD4+ and DR+CD8+ subsets and in T cells expressing several T cell receptor (TCR) Vb+ cells, perhaps representing Vb-specific T cell activation by MRSA-derived superantigens (Kidney Int 1995 ; 47 : 207-2 16). Moreover, we tested levels of cytokines, T-lymphocy te subsets, natural killer NK cells, memory T cells, and the expression of IL-2 receptors in order to better understand the role of bacterial superantigens and cytokines in the pathogenesis of MRSA- associated GN.
Methods. Twenty-two patients with MRSA infection who later developed glomerulonephritis (GN) caused by staphylococcal enterotoxin were evaluated immunologically in comparison with patients whose MRSA infection was not followed by GN (non-GN group) and normal individuals.
Results. Among peripheral lymphocytes, frequency of T cells expressing several TCR Vb's, especially Vb5-family TCR was higher in GN group than in the non-GN group as well as in normal healthy control. GN patients also showed increased serum levels of several cytokines, including tumor necrosis factor-a, interleukin-1b (IL-1b), IL-2, IL-6, IL-8, and IL-l0, which have been suggested to be responsible for the onset of nephritis. Memory cells, and IL-2 receptors also were elevated in GN group than in normal individuals.
Conclusion, These results suggest that T cells activated by MRSA-derived staphylococcal enterotoxins and subsequent production of cytokines may play important roles in the pathogenesis of MRSA-associated GN.
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