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变形链球菌可诱导严重龋齿大鼠产生 IgA 肾病样肾小球肾炎。

Streptococcus mutans induces IgA nephropathy-like glomerulonephritis in rats with severe dental caries.

机构信息

Department of Pediatric Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.

Department of Pediatric Dentistry, Division of Oral Infection and Disease Control, Osaka University Graduate School of Dentistry, Suita, Osaka, Japan.

出版信息

Sci Rep. 2021 Mar 11;11(1):5784. doi: 10.1038/s41598-021-85196-4.

Abstract

The mechanisms underlying immunoglobulin A nephropathy (IgAN), the most common chronic form of primary glomerulonephritis, remain poorly understood. Streptococcus mutans, a Gram-positive facultatively anaerobic oral bacterium, is a common cause of dental caries. In previous studies, S. mutans isolates that express Cnm protein on their cell surface were frequently detected in IgAN patients. In the present study, inoculation of Cnm-positive S. mutans in the oral cavities of 2-week-old specific-pathogen free Sprague-Dawley rats fed a high-sucrose diet for 32 weeks produced severe dental caries in all rats. Immunohistochemical analyses of the kidneys using IgA- and complement C3-specific antibodies revealed positive staining in the mesangial region. Scanning electron microscopy revealed a wide distribution of electron dense deposits in the mesangial region and periodic acid-Schiff staining demonstrated prominent proliferation of mesangial cells and mesangial matrix. These results suggest that IgAN-like glomerulonephritis was induced in rats with severe dental caries by Cnm-positive S. mutans.

摘要

免疫球蛋白 A 肾病(IgAN)是最常见的原发性肾小球肾炎的慢性形式,其发病机制仍知之甚少。变形链球菌是一种革兰阳性兼性厌氧口腔细菌,是龋齿的常见病因。在以前的研究中,在 IgAN 患者中经常检测到在其细胞表面表达 Cnm 蛋白的变形链球菌分离株。在本研究中,将 Cnm 阳性变形链球菌接种于 2 周龄无特定病原体 Sprague-Dawley 大鼠的口腔中,并用高蔗糖饮食喂养 32 周,所有大鼠均产生严重的龋齿。使用 IgA 和补体 C3 特异性抗体对肾脏进行免疫组织化学分析显示在系膜区呈阳性染色。扫描电子显微镜显示在系膜区有广泛分布的电子致密沉积物,过碘酸希夫染色显示系膜细胞和系膜基质明显增生。这些结果表明,严重龋齿的 Cnm 阳性变形链球菌可在大鼠中诱导 IgAN 样肾小球肾炎。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a41/7952735/2bf11ed991b8/41598_2021_85196_Fig1_HTML.jpg

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