Cytokines and T-cell responses in superantigen-related glomerulonephritis following methicillin-resistant Staphylococcus aureus infection.

Cytokines and T-cell responses in superantigen-related glomerulonephritis following methicillin-resistant Staphylococcus aureus infection.
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DOI:
10.1093/ndt/15.8.1170
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发表时间:
2000-08
期刊:
Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association
影响因子:
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通讯作者:
K. Yoh;M. Kobayashi;N. Yamaguchi;K. Hirayama;T. Ishizu;S. Kikuchi;S. Iwabuchi;K. Muro;S. Nagase;K. Aoyagi;M. Kondoh;K. Takemura;K. Yamagata;A. Koyama
K. Yoh;M. Kobayashi;N. Yamaguchi;K. Hirayama;T. Ishizu;S. Kikuchi;S. Iwabuchi;K. Muro;S. Nagase;K. Aoyagi;M. Kondoh;K. Takemura;K. Yamagata;A. Koyama
中科院分区:
其他
文献类型:
--
作者:
K. Yoh;M. Kobayashi;N. Yamaguchi;K. Hirayama;T. Ishizu;S. Kikuchi;S. Iwabuchi;K. Muro;S. Nagase;K. Aoyagi;M. Kondoh;K. Takemura;K. Yamagata;A. Koyama

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研究背景我们曾报道10例甲氧西林耐药金黄色葡萄球菌(MRSA)感染相关的肾小球肾炎(GN)患者的T细胞中DR+CD4+和DR+CD8+亚群以及表达多种T细胞受体(TCR)Vβ+细胞的T细胞显著增加,可能代表MRSA来源的超抗原对Vβ特异性T细胞的激活(Kidney Int 1995;47:207-216)。在本研究中,我们检测了细胞因子水平、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,以更好地了解细菌超抗原和细胞因子在MRSA相关性肾炎发病机制中的作用。方法对22例金黄色葡萄球菌肠毒素所致肾炎患者进行免疫学检测,并与未发生肾炎的患者(非肾炎组)及正常人进行比较。结果在外周血淋巴细胞中,GN组T细胞表达多种TCRVβ的频率明显高于非GN组和正常对照组,尤其是Vβ5家族TCR。肾小球肾炎患者血清中肿瘤坏死因子-α、白介素1-β、白介素2、白介素6、白介素8、白介素10等细胞因子水平也升高,与肾炎的发病有关。GN组记忆细胞和IL-2受体水平也明显升高。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相关性肾炎的发病机制中起重要作用。
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 DR+CD4+ and DR+CD8+ subsets of T cells and in T cells expressing several T-cell receptor (TCR) V beta+cells, perhaps representing V beta-specific T-cell activation by MRSA-derived superantigens (Kidney Int 1995; 47: 207-216). In this study we examine cytokine levels, T-lymphocyte 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 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, the frequency of T cells expressing several TCR V betas, especially V beta 5-family TCR, was higher in the GN group than in both the non-GN group and the normal healthy control group. GN patients also showed increased serum levels of several cytokines, including tumour necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), IL-2, IL-6, IL-8, and IL-10, which have been implicated in the onset of nephritis. Memory cells, and IL-2 receptors also were elevated in the GN group. CONCLUSION These results suggest that T cells activated by MRSA-derived staphylococcal enterotoxins and subsequent production of cytokines may play an important role in the pathogenesis of MRSA-associated GN.