Adhesion mechanism of Streptococcus anginosus to mucosal epithelial cells
Abstract number: P1979
Kodama Y., Sasaki M., Shimoyama Y., Tajika S., Kimura S.
Objective: Although Streptococcus anginosus is a part of the normal flora found in human dental plaque, recent studies indicate that S. anginosus infection in oral mucosa can be associated with oral squamous cell carcinoma. The organism possesses a number of pathogenic properties, however, adhesive mechanism that mediate the initial process of S. anginosus infection to oral mucosal epithelial cells remained to be elucidated. In this study, the adhesive abilities of S. anginosus to mucosal epithelial cells of a human larynx carcinoma cell line (HEp-2 cells) and a gingival epithelial cell line (GE1 cells) as well as the immobilized fibronectin were investigated.
Methods:S. anginosus ATCC 10713 and clinical isolates were used. The adhesive ability of S. anginosus was assessed by binding of bacteria to the cultured epithelial cells, and the immobilized extracellular matrix proteins. The fibronectin expression of HEp-2 cells was analyzed by Western blotting and RT-PCR assay.
Results:S. anginosus can adhere to both mucosal epithelial cells as other oral streptococci do. The adhesive ability could be ascribable to mainly its fibronectin-mediated adherence to the mucosal epithelial cells. It was also indicated that the adhesive ability to HEp-2 cells of the S. anginosus isolates from oral cancer tissues was significantly higher than that of the isolates from the plaque sample of healthy subjects. The cell-surface expression of fibronectin in HEp-2 cells was augmented by the bacterial adhesion itself and the autocrine activation of TGF-b1 induced by the bacterial adhesion. Furthermore, the addition of exogenous fibronectin (10 nM) enhanced the S. anginosus adherence to HEp-2 cells. The pretreatments with fibronectin of the bacterial cells as well as HEp-2 cells enhanced the S. anginosus adherence, and the enhancements were abrogated by the addition of anti-fibronectin antibodies, suggesting the coexistence of a direct adhesion of S. anginosus to the fibronectin of HEp-2 cell surfaces and another fibronectin-mediated adhesion mechanism involving a fibronectin bridge between the S. anginosus fibronectin-binding molecule(s) and the integrins of HEp-2 cells.
Conclusion: The present findings suggest that S. anginosus could adhere to mucosal epithelial cells via multiple adhesion mechanisms, and the adhesive ability to fibronectin could be involved in the pathogenicity of S. anginosus, leading to the onset of oral squamous cell carcinoma.
|Session name:||Abstracts 20th European Congress of Clinical Microbiology and Infectious Diseases|
|Location:||Vienna, Austria, 10 - 13 April 2010|
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