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Intravenous administration of Streptococcus mutans induces IgA nephropathy-like lesions
BACKGROUND: IgA nephropathy (IgAN) is one of the most frequently occurring types of chronic glomerulonephritis. Previous analyses have revealed that a major pathogen of dental caries, Streptococcus mutans [which expresses collagen-binding protein (Cnm) on its surface], is involved in the pathogenesi...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Springer Singapore
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7599197/ https://www.ncbi.nlm.nih.gov/pubmed/32909181 http://dx.doi.org/10.1007/s10157-020-01961-1 |
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author | Naka, Shuhei Wato, Kaoruko Misaki, Taro Ito, Seigo Nagasawa, Yasuyuki Nomura, Ryota Matsumoto-Nakano, Michiyo Nakano, Kazuhiko |
author_facet | Naka, Shuhei Wato, Kaoruko Misaki, Taro Ito, Seigo Nagasawa, Yasuyuki Nomura, Ryota Matsumoto-Nakano, Michiyo Nakano, Kazuhiko |
author_sort | Naka, Shuhei |
collection | PubMed |
description | BACKGROUND: IgA nephropathy (IgAN) is one of the most frequently occurring types of chronic glomerulonephritis. Previous analyses have revealed that a major pathogen of dental caries, Streptococcus mutans [which expresses collagen-binding protein (Cnm) on its surface], is involved in the pathogenesis of IgAN. METHODS: Cnm-positive S. mutans isolated from a patient with IgAN was intravenously administered to specific pathogen-free Sprague–Dawley rats to evaluate their kidney conditions. RESULTS: The urinary protein level of the S. mutans group reached a plateau at 30 days, with increased numbers of mesangial cells and an increased mesangial matrix. The numbers of rats with IgA-positive and/or C3-positive glomeruli were significantly greater in the S. mutans group than in the control group at 45 days (P < 0.05). Electron microscopy analyses revealed electron-dense depositions in the mesangial area among rats in the S. mutans group. There were significantly more CD68-positive cells (macrophages) in the glomeruli of the S. mutans group than in the glomeruli of the control group during the late phase (P < 0.05), similar to the findings in patients with IgAN. CONCLUSION: Our results suggested that intravenous administration of Cnm-positive S. mutans caused transient induction of IgAN-like lesions in rats. |
format | Online Article Text |
id | pubmed-7599197 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Springer Singapore |
record_format | MEDLINE/PubMed |
spelling | pubmed-75991972020-11-10 Intravenous administration of Streptococcus mutans induces IgA nephropathy-like lesions Naka, Shuhei Wato, Kaoruko Misaki, Taro Ito, Seigo Nagasawa, Yasuyuki Nomura, Ryota Matsumoto-Nakano, Michiyo Nakano, Kazuhiko Clin Exp Nephrol Original Article BACKGROUND: IgA nephropathy (IgAN) is one of the most frequently occurring types of chronic glomerulonephritis. Previous analyses have revealed that a major pathogen of dental caries, Streptococcus mutans [which expresses collagen-binding protein (Cnm) on its surface], is involved in the pathogenesis of IgAN. METHODS: Cnm-positive S. mutans isolated from a patient with IgAN was intravenously administered to specific pathogen-free Sprague–Dawley rats to evaluate their kidney conditions. RESULTS: The urinary protein level of the S. mutans group reached a plateau at 30 days, with increased numbers of mesangial cells and an increased mesangial matrix. The numbers of rats with IgA-positive and/or C3-positive glomeruli were significantly greater in the S. mutans group than in the control group at 45 days (P < 0.05). Electron microscopy analyses revealed electron-dense depositions in the mesangial area among rats in the S. mutans group. There were significantly more CD68-positive cells (macrophages) in the glomeruli of the S. mutans group than in the glomeruli of the control group during the late phase (P < 0.05), similar to the findings in patients with IgAN. CONCLUSION: Our results suggested that intravenous administration of Cnm-positive S. mutans caused transient induction of IgAN-like lesions in rats. Springer Singapore 2020-09-09 2020 /pmc/articles/PMC7599197/ /pubmed/32909181 http://dx.doi.org/10.1007/s10157-020-01961-1 Text en © The Author(s) 2020 Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Original Article Naka, Shuhei Wato, Kaoruko Misaki, Taro Ito, Seigo Nagasawa, Yasuyuki Nomura, Ryota Matsumoto-Nakano, Michiyo Nakano, Kazuhiko Intravenous administration of Streptococcus mutans induces IgA nephropathy-like lesions |
title | Intravenous administration of Streptococcus mutans induces IgA nephropathy-like lesions |
title_full | Intravenous administration of Streptococcus mutans induces IgA nephropathy-like lesions |
title_fullStr | Intravenous administration of Streptococcus mutans induces IgA nephropathy-like lesions |
title_full_unstemmed | Intravenous administration of Streptococcus mutans induces IgA nephropathy-like lesions |
title_short | Intravenous administration of Streptococcus mutans induces IgA nephropathy-like lesions |
title_sort | intravenous administration of streptococcus mutans induces iga nephropathy-like lesions |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7599197/ https://www.ncbi.nlm.nih.gov/pubmed/32909181 http://dx.doi.org/10.1007/s10157-020-01961-1 |
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