Streptococcus mutans with Collagen-Binding Protein: From Oral Cavity to Brain

2018 ◽  
Vol 115 ◽  
pp. 486
Author(s):  
Sundara Krishnan ◽  
Varidh Katiyar ◽  
Manoj Phalak ◽  
Ravi Sharma
2018 ◽  
Vol 115 ◽  
pp. 487
Author(s):  
Tokutaro Tanaka ◽  
Ryota Nomura ◽  
Kazuya Hokamura ◽  
Toshimitsu Hamasaki ◽  
Chikanori Inenaga ◽  
...  

2018 ◽  
Vol 113 ◽  
pp. e77-e81 ◽  
Author(s):  
Chikanori Inenaga ◽  
Kazuya Hokamura ◽  
Kazuhiko Nakano ◽  
Ryota Nomura ◽  
Shuhei Naka ◽  
...  

2014 ◽  
Vol 19 (5) ◽  
pp. 844-850 ◽  
Author(s):  
Taro Misaki ◽  
Shuhei Naka ◽  
Keiko Kuroda ◽  
Ryota Nomura ◽  
Tempei Shiooka ◽  
...  

2012 ◽  
Vol 27 (4) ◽  
pp. 308-323 ◽  
Author(s):  
R. Nomura ◽  
K. Nakano ◽  
S. Naka ◽  
H. Nemoto ◽  
K. Masuda ◽  
...  

2013 ◽  
Vol 58 (8) ◽  
pp. 989-996 ◽  
Author(s):  
Jinthana Lapirattanakul ◽  
Ryota Nomura ◽  
Hirotoshi Nemoto ◽  
Shuhei Naka ◽  
Takashi Ooshima ◽  
...  

2011 ◽  
Vol 2 (1) ◽  
Author(s):  
Kazuhiko Nakano ◽  
Kazuya Hokamura ◽  
Naho Taniguchi ◽  
Koichiro Wada ◽  
Chiho Kudo ◽  
...  

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Ryota Nomura ◽  
Masatoshi Otsugu ◽  
Masakazu Hamada ◽  
Saaya Matayoshi ◽  
Noboru Teramoto ◽  
...  

Abstract Streptococcus mutans, a significant contributor to dental caries, is occasionally isolated from the blood of patients with infective endocarditis. We previously showed that S. mutans strains expressing collagen-binding protein (Cnm) are present in the oral cavity of approximately 10–20% of humans and that they can effectively invade human umbilical vein endothelial cells (HUVECs). Here, we investigated the potential molecular mechanisms of HUVEC invasion by Cnm-positive S. mutans. The ability of Cnm-positive S. mutans to invade HUVECs was significantly increased by the presence of serum, purified type IV collagen, and fibrinogen (p < 0.001). Microarray analyses of HUVECs infected by Cnm-positive or -negative S. mutans strains identified several transcripts that were differentially upregulated during invasion, including those encoding the small G protein regulatory proteins ARHGEF38 and ARHGAP9. Upregulation of these proteins occurred during invasion only in the presence of serum. Knockdown of ARHGEF38 strongly reduced HUVEC invasion by Cnm-positive S. mutans. In a rat model of infective endocarditis, cardiac endothelial cell damage was more prominent following infection with a Cnm-positive strain compared with a Cnm-negative strain. These results suggest that the type IV collagen–Cnm–ARHGEF38 pathway may play a crucial role in the pathogenesis of infective endocarditis.


2015 ◽  
Vol 83 (5) ◽  
pp. 2001-2010 ◽  
Author(s):  
James H. Miller ◽  
Alejandro Avilés-Reyes ◽  
Kathy Scott-Anne ◽  
Stacy Gregoire ◽  
Gene E. Watson ◽  
...  

Streptococcus mutansis the etiological agent of dental caries and one of the many bacterial species implicated in infective endocarditis. The expression of the collagen-binding protein Cnm byS. mutanshas been associated with extraoral infections, but its relevance for dental caries has only been theorized to date. Due to the collagenous composition of dentinal and root tissues, we hypothesized that Cnm may facilitate the colonization of these surfaces, thereby enhancing the pathogenic potential ofS. mutansin advancing carious lesions. As shown for extraoral endothelial cell lines, Cnm mediates the invasion of oral keratinocytes and fibroblasts byS. mutans. In this study, we show that in the Cnm+native strain, OMZ175, Cnm mediates stringent adhesion to dentinal and root tissues as well as collagen-coated surfaces and promotes both cariogenicity and carriagein vivo. In vitro,ex vivo, andin vivoexperiments revealed that while Cnm is not universally required forS. mutanscariogenicity, it contributes to (i) the invasion of the oral epithelium, (ii) enhanced binding on collagenous surfaces, (iii) implantation of oral biofilms, and (IV) the severity of caries due to a native Cnm+isolate. Taken together, our findings reveal that Cnm is a colonization factor that contributes to the pathogenicity of certainS. mutansstrains in their native habitat, the oral cavity.


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