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Abstract: SA-PO599

Intravenous Infection with Cnm-Positive Streptococcus mutans, a Dental Pathogen, Induces IgA Nephropathy-Like Lesions in Rats

Session Information

Category: Glomerular Diseases

  • 1202 Glomerular Diseases: Immunology and Inflammation

Authors

  • Misaki, Taro, Seirei Hamamatsu General Hospital, Hamamatsu, Japan
  • Naka, Shuhei, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan
  • Wato, Kaoruko, Osaka University Graduate School of Dentistry, Suita, Japan
  • Shimizu, Yoshitaka, Seirei Hamamatsu General Hospital, Hamamatsu, Japan
  • Nagasawa, Yasuyuki, Hyogo College of Medicine, Nishinomiya, Japan
  • Ito, Seigo, National Defense Medical College, Tokorozawa, Japan
  • Nomura, Ryota, Osaka University Graduate School of Dentistry, Suita, Japan
  • Matsumoto-Nakano, Michiyo, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan
  • Nakano, Kazuhiko, Osaka University Graduate School of Dentistry, Suita, Japan
Background

IgA nephropathy (IgAN) is one of most common types of primary glomerulonephritis worldwide, but its precise pathogenesis remains unclear. Previously, we reported that Streptococcus mutans, a major pathogen of dental caries was frequently isolated from the oral cavity of IgAN patients; these isolates showed surface expression of collagen-binding protein (Cnm). However, there is no direct evidence that Cnm-positive S. mutans induces IgAN. In the present study, we evaluated renal lesions in rats that were intravenously infected with Cnm-positive S. mutans isolated from an IgAN patient.

Methods

Cnm-positive S. mutans strain SN74, isolated from the saliva of an IgAN patient, was intravenously administered to 4-week-old male specific pathogen-free Sprague-Dawley rats. At 15, 30, 45, and 60 days post-infection, kidney specimens were evaluated. Periodic acid-Schiff staining and fluorescent immunostaining with IgA, C3, and CD68 antibodies was performed; electron microscopy analysis was also performed.

Results

Proteinuria in the S. mutans group was significantly elevated, compared with that in the control group at 30 days post-infection (p < 0.05). Histopathological examinations revealed increased presence of mesangial cells and matrix at 30 days post-infection in the S. mutans group. Immunochemical examinations demonstrated that combined IgA/C3 deposition in mesangial cells was significantly greater in the S. mutans group than in the control group at 45 days post-infection (p < 0.05). Electron microscopy analysis showed electron-dense deposits in the mesangial area and hump in subepithelial areas in the S. mutans group at 45 days post-infection. Furthermore, the numbers of CD68-positive cells (i.e., macrophages) in the glomeruli of the S. mutans group were significantly higher than those in the control group at 30, 45, and 60 days post-infection (p < 0.01).

Conclusion

Intravenous infection with Cnm-positive S. mutans isolated from an IgAN patient could induce IgAN or infection-related glomerulonephritis in rats.