Papers

Dec, 2020

Intravenous administration of Streptococcus mutans induces IgA nephropathy-like lesions.

Clinical and experimental nephrology
  • Shuhei Naka
  • ,
  • Kaoruko Wato
  • ,
  • Taro Misaki
  • ,
  • Seigo Ito
  • ,
  • Yasuyuki Nagasawa
  • ,
  • Ryota Nomura
  • ,
  • Michiyo Matsumoto-Nakano
  • ,
  • Kazuhiko Nakano

Volume
24
Number
12
First page
1122
Last page
1131
Language
English
Publishing type
Research paper (scientific journal)
DOI
10.1007/s10157-020-01961-1

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.

Link information
DOI
https://doi.org/10.1007/s10157-020-01961-1
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/32909181
PubMed Central
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7599197
ID information
  • DOI : 10.1007/s10157-020-01961-1
  • Pubmed ID : 32909181
  • Pubmed Central ID : PMC7599197

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