变形链球菌胶原结合蛋白Cnm对大鼠IgA肾病样肾炎的影响-动脉网

Contribution of collagen-binding protein Cnm of Streptococcus mutans to induced IgA nephropathy-like nephritis in rats

Nature 等信源发布 2024-09-14 19:43

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AbstractIgA nephropathy (IgAN), the most common primary glomerulonephritis, is considered an intractable disease with unknown pathogenic factors. In our previous study, Streptococcus mutans, the major causative bacteria of dental caries, which expresses Cnm, was related to the induction of IgAN-like nephritis.

摘要IgA肾病（IgAN）是最常见的原发性肾小球肾炎，被认为是一种致病因素未知的难治性疾病。在我们之前的研究中，表达Cnm的龋齿主要致病细菌变形链球菌与IgAN样肾炎的诱导有关。

In the present study, the Cnm-positive S. mutans parental strain, a Cnm-defective isogenic mutant strain, its complementation strain, and recombinant Cnm (rCnm) protein were administered intravenously to Sprague Dawley rats, and the condition of their kidneys was evaluated focusing on the pathogenicity of Cnm.

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Rats treated with parental and complement bacterial strains and rCnm protein developed IgAN-like nephritis with mesangial proliferation and IgA and C3 mesangial deposition. Scanning immunoelectron microscopy revealed that rCnm was present in the electron-dense deposition area of the mesangial region in the rCnm protein group.

用亲本和补体细菌菌株和rCnm蛋白治疗的大鼠发生IgAN样肾炎，伴有系膜增生和IgA和C3系膜沉积。扫描免疫电镜显示，rCnm蛋白组系膜区的电子致密沉积区存在rCnm。

These results demonstrated that the Cnm protein itself is an important factor in the induction of IgAN in rats..

这些结果表明，Cnm蛋白本身是诱导大鼠IgAN的重要因素。。

IntroductionIgA nephropathy (IgAN), the most common primary glomerulonephritis, is considered an intractable disease with various pathogenetic factors1,2,3. Over approximately 20 years from the onset of disease, 30–40% of patients develop terminal renal failure1,2,3,4. Common clinical findings include proteinuria and hematuria, but a renal biopsy is considered essential to confirm a diagnosis5,6,7.

引言IgA肾病（IgAN）是最常见的原发性肾小球肾炎，被认为是一种具有多种致病因素的难治性疾病1,2,3。在疾病发作后约20年内，30-40%的患者发展为终末期肾衰竭1,2,3,4。常见的临床表现包括蛋白尿和血尿，但肾活检被认为是确诊的必要条件5,6,7。

The diagnostic hallmark of IgAN is the predominance of IgA deposits, either alone or with IgG, IgM, or both, in the glomerular mesangial regions8. More than 90% of IgAN patients have complement C3 deposition in their glomeruli9. Most C3 is present in the mesangial and paramesangial regions including some vascular endothelial cells2,10.

IgAN的诊断标志是在肾小球系膜区域单独或与IgG，IgM或两者同时存在的IgA沉积物占优势8。超过90%的IgAN患者肾小球中有补体C3沉积9。大多数C3存在于系膜和血管旁区域，包括一些血管内皮细胞2,10。

Typical histopathological findings in patients with IgAN include increased numbers of mesangial cells and matrix in the mesangial region as well as the deposition of immune complexes11. Patients with IgAN sometimes present with macroscopic hematuria when they have an upper respiratory tract infection, such as tonsillitis12.

IgAN患者的典型组织病理学发现包括系膜区系膜细胞和基质数量增加以及免疫复合物的沉积11。IgAN患者在上呼吸道感染（如扁桃体炎）时有时会出现肉眼血尿12。

Several bacterial species have been reported to be potential factors involved in the pathogenesis of IgAN13,14,15,16,17, including dental caries-related bacteria18,19,20,21,22,23,24,25 and periodontitis-related bacteria26,27,28.Streptococcus mutans, the major causative bacteria of dental caries, is a Gram-positive, facultative anaerobic bacteria29, which can induce infective endocarditis by invading the bloodstream during invasive dental procedures, such as tooth extractions30.

据报道，几种细菌种类是参与IgAN13,14,15,16,17发病机制的潜在因素，包括龋齿相关细菌18,19,20,21,22,23,24,25和牙周炎相关细菌26,27,28.Streptococcus mutans是龋齿的主要致病细菌，是一种革兰氏阳性兼性厌氧细菌29，可通过在侵入性牙科手术（如拔牙）期间侵入血流来诱发感染性心内膜炎30。

A collagen-binding protein (Cnm) of approximately 120 kDa is expressed on the surface of some S. mutans strains31 and is involved in adhesion to and invasion of vascular endothelial cells, indicating it might be an important factor that causes infecti.

大约120 kDa的胶原结合蛋白（Cnm）在一些变形链球菌菌株31的表面上表达，并参与血管内皮细胞的粘附和侵袭，表明它可能是导致感染的重要因素。

Data availability

数据可用性

The data that support the findings of this study are available from the corresponding author upon request. The source data underlying Figs. 1, 2, 6, Supplementary Fig. 1, and Table 1, Supplementary Table 1. These source data are listed in Supplementary Data 1.

支持本研究结果的数据可应要求从通讯作者处获得。图1、2、6（补充图1）和表1（补充表1）的源数据。这些源数据列在补充数据1中。

Materials availability

材料可用性

Correspondence and requests for materials should be addressed to Michiyo Matsumoto-Nakano.

信件和材料要求应寄给松本美雄。

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Download referencesAcknowledgementsThis work was supported by funding from JSPS KAKENHI (grant numbers 20K10225, 21KK0160, 21H03149, 23K09146, 23K09435, 23K27805 24K02650). We thank Yumiko Morishita, Mika Monobe, and Miki Kajino (Central Research Laboratory, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences) for assistance with preparing tissue segments.

下载参考文献致谢这项工作得到了JSPS KAKENHI的资助（资助号20K10225、21KK0160、21H03149、23K09146、23K09435、23K27805、24K02650）。我们感谢森下Yumiko Morishita，Mika Monobe和Miki Kajino（冈山大学医学，牙科和药物科学研究生院中央研究实验室）为准备组织切片提供的帮助。

We thank Masumi Furutani and Moemi Tsukano (Central Research Laboratory, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences) for assistance with electron microscopic analyses. We thank Mitchell Arico and J. Ludovic Croxford, PhD, from Edanz (https://jp.edanz.com/ac) for editing a draft of this manuscript.Author informationAuthor notesThese authors contributed equally: Shuhei Naka, Daiki Matsuoka.Authors and AffiliationsDepartment of Pediatric Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Okayama, JapanShuhei Naka, Daiki Matsuoka & Michiyo Matsumoto-NakanoDivision of Nephrology, Seirei Hamamatsu General Hospital, Hamamatsu, Shizuoka, JapanTaro MisakiDepartment of Nursing, Faculty of Nursing, Seirei Christopher University, Hamamatsu, Shizuoka, JapanTaro MisakiDepartment of General Internal Medicine, Hyogo College of Medicine, Nishinomiya, Hyogo, JapanYasuyuki NagasawaDepartment of Internal Medicine, Japan Self-Defense Force Iruma Hospital, Saitama, JapanSeigo ItoDepartment of Pediatric Dentistry, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, JapanRyota NomuraDepartment of Pediatric Dentistry, Graduate School of Dentistry, The University of Osaka, Suita, Osaka, JapanKazuhiko NakanoAuthorsShuhei NakaView author publicationsYou can also sear.

我们感谢Masumi Furutani和Moemi Tsukano（冈山大学医学，牙科和制药科学研究生院中央研究实验室）对电子显微镜分析的帮助。我们感谢来自Edanz的Mitchell Arico和J.Ludovic Croxford博士(https://jp.edanz.com/ac)编辑这份手稿的草稿。作者信息作者注意到这些作者做出了同样的贡献：Shuhei Naka，Daiki Matsuoka。作者和附属机构冈山大学医学、牙科和药物科学研究生院儿科牙科系，冈山，冈山，日本中平，大木松冈和松本美雄，日本静冈，日本静冈，滨松总医院，日本静冈，静冈，静冈，静冈，静冈，静冈，静冈，日本静冈，静冈，静冈，静冈，静冈内科，日本自卫队Iruma医院，Saitama，JapanSeigo Ito广岛大学生物医学与健康科学研究生院儿科牙科，广岛，日本野村，大阪大学牙科研究生院儿科牙科，大阪，Suita，JapanKazuhiko NakanoAuthorsShuhei NakaView作者出版物您也可以搜索。

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PubMed谷歌ScholarTaro MisakiView作者出版物您也可以在中搜索此作者。的信息。的研究报告中找到该作者。的信息。的研究报告。的研究报告。的研究报告中，该研究报告的作者为美国的一个研究机构，该机构的研究人员在其研究报告

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PubMed Google ScholarContributionsS.N. and D.M. designed the study under the supervision of M.M.N. and K.N. S.N., D.M., T.M., Y.N., S.I. and M.M.N. performed the animal experiments. Statistical analyses and data interpretation were performed by S.N., D.M., T.M., S.I., R.N. and K.N.

PubMed谷歌学术贡献。N、 D.M.在M.M.N.和K.N.S.N.的监督下设计了这项研究，D.M.，T.M.，Y.N.，S.I.和M.M.N.进行了动物实验。统计分析和数据解释由S.N.，D.M.，T.M.，S.I.，R.N.和K.N.进行。

S.N., D.M., T.M., K.N. and M.M.N. wrote the manuscript and all authors approved the final version.Corresponding authorCorrespondence to.

S、 N.，D.M.，T.M.，K.N.和M.M.N.撰写了手稿，所有作者都批准了最终版本。对应作者对应。

Michiyo Matsumoto-Nakano.Ethics declarations

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Communications Biology thanks Jianbo Qing and the other, anonymous, reviewer for their contribution to the peer review of this work. Primary Handling Editors: Jesmond Dalli and Tobias Goris. A peer review file is available.

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Reprints and permissionsAbout this articleCite this articleNaka, S., Matsuoka, D., Misaki, T. et al. Contribution of collagen-binding protein Cnm of Streptococcus mutans to induced IgA nephropathy-like nephritis in rats.

转载和许可本文引用本文Naka，S.，Matsuoka，D.，Misaki，T。等人。变形链球菌的胶原结合蛋白Cnm对大鼠诱导的IgA肾病样肾炎的贡献。

Commun Biol 7, 1141 (2024). https://doi.org/10.1038/s42003-024-06826-xDownload citationReceived: 07 November 2023Accepted: 03 September 2024Published: 14 September 2024DOI: https://doi.org/10.1038/s42003-024-06826-xShare this articleAnyone you share the following link with will be able to read this content:Get shareable linkSorry, a shareable link is not currently available for this article.Copy to clipboard.

Commun Biol 71141（2024）。https://doi.org/10.1038/s42003-024-06826-xDownload引文收到日期：2023年11月7日接受日期：2024年9月3日发布日期：2024年9月14日OI：https://doi.org/10.1038/s42003-024-06826-xShare本文与您共享以下链接的任何人都可以阅读此内容：获取可共享链接对不起，本文目前没有可共享的链接。复制到剪贴板。

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