Intravenous administration of Streptococcus mutans induces IgA nephropathy-like lesions.
Animals
Antigens, CD
/ metabolism
Antigens, Differentiation, Myelomonocytic
/ metabolism
Complement C3
/ metabolism
Disease Models, Animal
Glomerulonephritis, IGA
/ immunology
Humans
Immunoglobulin A
/ metabolism
Kidney
/ immunology
Macrophages
/ immunology
Male
Rats, Sprague-Dawley
Streptococcal Infections
/ complications
Streptococcus mutans
/ isolation & purification
Time Factors
Dental caries
Glomerulonephritis
IgA nephropathy
Intravenous administration
Rats
Streptococcus mutans
Journal
Clinical and experimental nephrology
ISSN: 1437-7799
Titre abrégé: Clin Exp Nephrol
Pays: Japan
ID NLM: 9709923
Informations de publication
Date de publication:
Dec 2020
Dec 2020
Historique:
received:
15
07
2020
accepted:
17
08
2020
pubmed:
11
9
2020
medline:
25
8
2021
entrez:
10
9
2020
Statut:
ppublish
Résumé
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. 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. 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. Our results suggested that intravenous administration of Cnm-positive S. mutans caused transient induction of IgAN-like lesions in rats.
Sections du résumé
BACKGROUND
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
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
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
CONCLUSIONS
Our results suggested that intravenous administration of Cnm-positive S. mutans caused transient induction of IgAN-like lesions in rats.
Identifiants
pubmed: 32909181
doi: 10.1007/s10157-020-01961-1
pii: 10.1007/s10157-020-01961-1
pmc: PMC7599197
doi:
Substances chimiques
Antigens, CD
0
Antigens, Differentiation, Myelomonocytic
0
CD68 protein, rat
0
Complement C3
0
Immunoglobulin A
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1122-1131Subventions
Organisme : Japan Society for Promotion of Science
ID : 17K11959
Organisme : Japan Society for Promotion of Science
ID : 19K10098
Organisme : Japan Society for Promotion of Science
ID : 18H03010
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