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Staphylococcus aureus antigens induce IgA-type glomerulonephritis in Balb/c mice

金黄色葡萄球菌抗原诱导 Balb/c 小鼠 IgA 型肾小球肾炎

基本信息

批准号：
13671096
负责人：
KOYAMA Akio
金额：
$ 2.43万
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：
2001
资助国家：
日本
起止时间：
2001 至 2002
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-13671096/
关键词：
Immunoglobulin A nephropathy mouse strains 30-35kDa protein Glomerular deposition of antigens Th1 & Th2 type IgA-production 免疫遺伝学的背景

项目摘要

Background. Staphylococcus aureus (S. aureus) is a common normal and pathogenic flora that colonizes on mucosal tissues. We had earlier reported glomerulonephritis occurred during methicillin resistant S. aureus infection, that showed polyclonal elevation of serum IgA and IgG levels and various histological findings, such as mesangial extracapillary and endocapillary proliferation. To investigate pathogenic roles of S.aureus antigens we induced IgA-type glomerulonephritis in mice which is similar to human IgA nephropathy, by immunization of antigens derived from S. aureus.Methods. BaIb/c mice (Th2 dominant type) and C57BL/6 (Th1 dominant type) were immunized with antigens deriired from S. aureus with Freund's incomplete adiuvant biweekly for 4 months.Results. Mesangial proliferative glomerulonephritis with IgA, IgG and C3 depositions were observed in all BaIb/c mice. Although C3 depositioris and cell proliferation in the mesangial area were also seen in C57BL/6 mice, they were not correlated with urinary findings. In BaIb/c mice, S. aureus antigens were detected in glomeruli using affinity purified human anti-S. aureus antibodies, however there was no staining in C57BL/6 mice. The used antibodies reacted with several S. aureus antigens. by western blot analysis and the main band that was differently recognized between BaIb/c and C57BL/6 was around 30-35kDa. Moreover increased transforming growth factor-β mRNA expression was seen in BaIb/c compare to those in B6.Conclusions. S. aureus antigens, especially 30-35kDa protein and genetic background of hosts may play important roles in the pathogenesis of IgA-like glomerulonephritis.

背景金黄色葡萄球菌(S.金黄色葡萄球菌）是在粘膜组织上定殖的常见的正常和致病植物群。我们早先报道了在耐甲氧西林S.金黄色葡萄球菌感染，其显示血清伊加和IgG水平的多克隆升高和各种组织学发现，例如系膜毛细血管外和毛细血管内增殖。为了研究金黄色葡萄球菌抗原的致病作用，我们通过免疫金黄色葡萄球菌抗原诱导小鼠IgA型肾小球肾炎，其与人伊加肾病相似。aureus.Methods.用S. pH7.1抗原分别免疫Th 2型（BaIb/c）小鼠和Th 1型（C57 BL/6）小鼠。结果：金黄色葡萄球菌感染组与对照组比较，差异有统计学意义（P < 0. 05）。在所有BaIb/c小鼠中均观察到系膜增生性肾小球肾炎伴伊加、IgG和C3沉积。尽管在C57 BL/6小鼠中也观察到系膜区C3沉积和细胞增殖，但它们与尿液检查结果无关。在BaIb/c小鼠中，S.用亲和纯化的人抗S.而在C57 BL/6小鼠中没有染色。所用的抗体与几个S.金黄色葡萄球菌抗原。经Western blot分析，BaIb/c与C57 BL/6的差异识别带主要在30- 35 kDa之间。与B6组相比，BaIb/c组TGF-β mRNA的表达明显增加。S.金黄色葡萄球菌抗原，特别是30- 35 kDa蛋白和宿主的遗传背景可能在IgA样肾炎的发病中起重要作用。