TY - JOUR
T1 - Intravenous administration of Streptococcus mutans induces IgA nephropathy-like lesions
AU - Naka, Shuhei
AU - Wato, Kaoruko
AU - Misaki, Taro
AU - Ito, Seigo
AU - Nagasawa, Yasuyuki
AU - Nomura, Ryota
AU - Matsumoto-Nakano, Michiyo
AU - Nakano, Kazuhiko
N1 - Funding Information:
This study was funded by Grants-in-aid for Scientific Research from the Japan Society for Promotion of Science (17K11959 to SN, 19K10098 to TM, and 18H03010 to KN). 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 sections; we thank Masumi Furutani (Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences) for assistance with electron microscopy analyses.
Funding Information:
This study was funded by Grants-in-aid for Scientific Research from the Japan Society for Promotion of Science (17K11959 to SN, 19K10098 to TM, and 18H03010 to KN). 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 sections; we thank Masumi Furutani (Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences) for assistance with electron microscopy analyses.
Publisher Copyright:
© 2020, The Author(s).
PY - 2020/12/1
Y1 - 2020/12/1
N2 - 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.
AB - 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.
KW - Dental caries
KW - Glomerulonephritis
KW - IgA nephropathy
KW - Intravenous administration
KW - Rats
KW - Streptococcus mutans
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U2 - 10.1007/s10157-020-01961-1
DO - 10.1007/s10157-020-01961-1
M3 - Article
C2 - 32909181
AN - SCOPUS:85090477598
SN - 1342-1751
VL - 24
SP - 1122
EP - 1131
JO - Clinical and Experimental Nephrology
JF - Clinical and Experimental Nephrology
IS - 12
ER -