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Browsing by Author "Quint, Nicole"
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Item Effects of Nicotine on Aerobic and Anaerobic Serotype K Streptococcus mutans Biofilm Formation(Office of the Vice Chancellor for Research, 2015-04-17) Quint, Nicole; Gomez, Grace; Gregory, Richard L.Atherosclerosis is a specific form of arteriosclerosis where the walls of arteries began to thicken as a result of bacterial invasion and accumulation of inflammatory white blood cells. There could be a direct correlation of atherosclerosis and the intake of nicotine. Nicotine has been reported to increase the amount of the cariogenic oral bacteria known as Streptococcus mutans; thus possibly leading to an increase of dental caries. Serotype K S. mutans has been associated strongly with atherosclerosis. Objective: This study focused on the biofilm formation of S. mutans serotype K when incubated in various dilutions of nicotine. Methods: S. mutans UA159 (stereotype C), and stereotype K strains 89, 52, and 51 were cultured in tryptic soy broth (TSB) overnight and then added to dilutions of TSB with 1% sucrose (TSBS) containing concentrations of nicotine between 0 and 32 mg/ml. Each dilution was added to 96-well microtiter plates, inoculated with bacteria and incubated for 24 hours aerobically at 37oC in 5% CO2 and anaerobically. The plates were treated with formaldehyde, crystal violet, and isopropanol and biofilm formation was measured at an absorbance of 490 nm. Results: Strains UA159, 89, 52, and 51 all demonstrated significantly higher biofilm formation (p<0.05) at a nicotine dilution of 8 mg/ml. When comparing the anaerobic results to the aerobic results, anaerobic incubation increased the overall biofilm formation across the majority of nicotine dilutions. Conclusion: It was established that when S. mutans strains UA159, 89, 52, and 51 were incubated anaerobically and aerobically biofilm formation was enhanced. Smoking can lead to a higher population of S. mutans in the oral cavity that potentially has traits of significantly enhanced biofilm formation when presented with moderately high levels of nicotine which may lead to increased binding to endothelial cells contributing to atherosclerosis.Item Serotype k Streptococcus mutans Binding to Collagen and Fibrinogen in Nicotine(Office of the Vice Chancellor for Research, 2016-04-08) Quint, Nicole; Gregory, Richard L.Background: Streptococcus mutans is a gram-positive coccus-shaped, facultatively anaerobic bacterium that is commonly found in the human oral cavity and is a major contributor to tooth decay. The bacterium has the potential to make its way into the blood stream and adhere to endothelial cell proteins such as collagen and fibrinogen in the arteries through specific receptors potentially leading to atherosclerosis. Endothelial cells secrete cell-associated and cell-free collagen and fibrinogen. Specifically, serotype k S. mutans have been associated with atherosclerosis and nicotine has been shown to increase the biofilm formation of S. mutans (serotype k). The focus of this research was to measure S. mutans ability to bind to collagen type I and fibrinogen when the cells were grown in the presence of nicotine. Methods: S. mutans serotype k strains 51, 52, and 89 were cultured in 0–2 mg/mL nicotine. Formaldehyde was added to kill the cells followed by labeling the cells with biotin. Collagen type I and fibrinogen were coated (1 μg/mL) onto 96-well microtiter plates. The plates were washed and 1% BSA was added to block the wells. Then the biotinylated nicotine-treated S. mutans were added, incubated to allow binding to the endothelial cell proteins, and washed. Finally, ExtrAvidin HRP and OPD were added to the plate and the optical density was measured at an absorbance of 490 nm. Results: The optical density was directly related to the relative number of cells bound to collagen type I and fibrinogen. Conclusion: The results demonstrated a significant increase in all three strains of S. mutans binding to the proteins when cultured in 1 and 2 mg/mL concentrations of nicotine compared to the 0 nicotine control. The increased numbers of nicotine-treated S. mutans binding to the endothelial cell proteins may have the ability to contribute to atherosclerosis.