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Studies on the pathogenesis of glomerulonephritis and vascultitis induced by superantigen.

超抗原诱导的肾小球肾炎和血管炎发病机制的研究。

基本信息

批准号：
09671147
负责人：
KOYAMA Akio
金额：
$ 2.24万
依托单位：
Institute of Clinical Medicine, University of Tsukuba
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1997
资助国家：
日本
起止时间：
1997 至 1998
项目状态：
已结题

项目摘要

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.

背景资料。我们先前报道了10例合并耐甲氧西林金黄色葡萄球菌(MRSA)感染的肾小球肾炎(GN)患者，其DR+CD4+和DR+CD8+亚群以及表达几种T细胞受体(TCR)VB+细胞的T细胞均显著增加，可能代表MRSA来源的超抗原对VB特异性T细胞的激活(Kidney Int 1995；47：207-216)。此外，我们还检测了细胞因子、T淋巴细胞亚群、自然杀伤细胞、记忆T细胞和IL-2受体的表达水平，以更好地了解细菌超抗原和细胞因子在MRSA相关GNs发病中的作用。对22例MRSA感染后发生葡萄球菌肠毒素所致肾小球肾炎(GN)的患者进行免疫学评估，并与未发生GN的患者(非GN组)和正常人进行比较。在外周血淋巴细胞中，GN组表达多种TCRVb的T细胞频率明显高于非GN组和正常对照组，尤其是Vb5家族TCR。GN患者血清中肿瘤坏死因子-a、白介素1b(IL-1b)、IL-2、IL-6、IL-8和IL-10等细胞因子水平也升高，提示它们与肾炎的发病有关。结论MRSA金黄色葡萄球菌肠毒素激活的T细胞及随后产生的细胞因子可能在MRSA相关性GN的发病机制中起重要作用。