Taro Misaki1, Shuhei Naka2, Keiko Kuroda2, Ryota Nomura2, Tempei Shiooka3, Yoshitaka Naito3, Yumiko Suzuki3, Hideo Yasuda4, Taisuke Isozaki3, Kazuhiko Nakano2. 1. Division of Nephrology, Seirei Hamamatsu General Hospital, 2-12-12 Sumiyoshi, Naka-ku, Hamamatsu, Shizuoka, 430-8558, Japan. misakitar@sis.seirei.or.jp. 2. Department of Pediatric Dentistry, Osaka University Graduate School of Dentistry, Osaka, Japan. 3. Division of Nephrology, Seirei Hamamatsu General Hospital, 2-12-12 Sumiyoshi, Naka-ku, Hamamatsu, Shizuoka, 430-8558, Japan. 4. First Department of Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Abstract
BACKGROUND: IgA nephropathy (IgAN) is the most common primary chronic glomerulonephritis; however, its precise initiating pathogenesis remains unclear. Streptococcus mutans is a major pathogen of human dental caries. S. mutans strains with the cnm gene encoding Cnm, a collagen-binding protein, have been reported to contribute to the development of systemic diseases. However, the contribution of S. mutans with Cnm in the development of IgAN has not been reported. The aim of this study was to investigate the prevalence of cnm-positive S. mutans in IgAN patients and clarify the effects of cnm-positive S. mutans on the histological pathology of IgAN. METHODS: We identified the cnm gene in S. mutans isolated in saliva specimens, which were collected from IgAN patients (n = 53) and control subjects (n = 50). We evaluated the collagen-binding properties of S. mutans in IgAN patients and controls. The clinical parameters and histological scores were also assessed in IgAN patients. RESULTS: The rates of S. mutans isolation in IgAN and control groups were 84.0 and 84.9 %, respectively, not significantly dfferent. cnm-positive strains were significantly more prevalent in the IgAN group than in controls (32.1 vs. 14.0 %, p < 0.05). With regard to collagen-binding assays, the binding rates of cnm-positive strains were significantly higher in the IgAN group than in controls (96.6 vs. 30.0, p < 0.05). In addition, the segmental glomerulosclerosis scores were significantly higher in cnm-positive patients with IgAN than in cnm-negative patients with IgAN (0.94 vs. 0.57, p < 0.05). CONCLUSION: cnm-positive S. mutans strains are potentially associated with the pathogenesis of IgAN.
BACKGROUND: IgA nephropathy (IgAN) is the most common primary chronic glomerulonephritis; however, its precise initiating pathogenesis remains unclear. Streptococcus mutans is a major pathogen of human dental caries. S. mutans strains with the cnm gene encoding Cnm, a collagen-binding protein, have been reported to contribute to the development of systemic diseases. However, the contribution of S. mutans with Cnm in the development of IgAN has not been reported. The aim of this study was to investigate the prevalence of cnm-positive S. mutans in IgANpatients and clarify the effects of cnm-positive S. mutans on the histological pathology of IgAN. METHODS: We identified the cnm gene in S. mutans isolated in saliva specimens, which were collected from IgANpatients (n = 53) and control subjects (n = 50). We evaluated the collagen-binding properties of S. mutans in IgANpatients and controls. The clinical parameters and histological scores were also assessed in IgANpatients. RESULTS: The rates of S. mutans isolation in IgAN and control groups were 84.0 and 84.9 %, respectively, not significantly dfferent. cnm-positive strains were significantly more prevalent in the IgAN group than in controls (32.1 vs. 14.0 %, p < 0.05). With regard to collagen-binding assays, the binding rates of cnm-positive strains were significantly higher in the IgAN group than in controls (96.6 vs. 30.0, p < 0.05). In addition, the segmental glomerulosclerosis scores were significantly higher in cnm-positive patients with IgAN than in cnm-negative patients with IgAN (0.94 vs. 0.57, p < 0.05). CONCLUSION:cnm-positive S. mutans strains are potentially associated with the pathogenesis of IgAN.
Entities:
Keywords:
Collagen-binding protein; IgA nephropathy; Streptococcus mutans; cnm
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