Streptococcus mutans Binding to Collagen, Fibrinogen, Fibronectin, and Laminin

Abstract

Introduction: Streptococcus mutans, nicotine, and certain proteins may be involved in a complicated mechanism that contributes to atherosclerosis. Build up of arterial plaque causes atherosclerosis. Arterial plaque is mainly composed of fat, cholesterol, and calcium. When plaque builds up in the arteries, a clot or blockage can occur and may cause an occlusion. Objective: S. mutans grows in oral biofilm and causes dental caries. These bacteria enter the blood stream from mucosal breaks in the oral cavity. There is evidence that S. mutans binds to endothelial cell surface proteins lining arterial surfaces. An increased incidence of S. mutans in arterial plaque seems to have a direct relationship with atherosclerosis. From preliminary research, there was a strong indication that increased S. mutans biofilm formation is caused by nicotine. The number of binding proteins on nicotine-treated S. mutans cell surface increases as well. In addition, results demonstrated that S. mutans binds to collagen type I, fibrinogen, fibronectin, and laminin, which are proteins found on endothelial cells. Methods: To investigate protein binding, S. mutans UA159 was cultured in 0, 0.25, 0.50, 1.0, 2.0, and 4.0 mg/ml of nicotine and their ability to bind to human collagen type I, fibrinogen, fibronectin and laminin was assessed using an ELISA assay. Results: S. mutans significantly bound to collagen type I and fibrinogen when cultured in 2 and 4 mg/ml nicotine. S. mutans significantly bound to laminin when the bacterium was grown in 1, 2, and 4 mg/ml. The binding of S. mutans to fibronectin varied when cultured in different concentrations of nicotine. Conclusion: From the results, it can be concluded that S. mutans UA159 binds to collagen type I, fibrinogen, fibronectin, and laminin. This indicates that S. mutans and the proteins studied are very likely to be part of the mechanism that leads to atherosclerosis.