PURPOSE:Smokers have increased denture stomatitis caused primarily by Candida albicans. The primary aim of this study was to demonstrate the impact of a wide range of nicotine and cigarette smoke condensate (CSC) concentrations on biofilm formation and metabolic activity of C. albicans on acrylic denture material. MATERIALS AND METHODS:C. albicans (ATCC strain 10231) was used. Standardized denture acrylic (PMMA) specimens (total of 135 specimens) were incubated with C. albicans and exposed to nicotine and CSC at different concentrations (0, 0.25, 0.5, 1, 2, 4, 8, 16, and 32 mg/ml) and (0, 0.25, 0.5, 1, 2, and 4 mg/ml), respectively. For each experiment, 3 samples per nicotine and CSC concentration and a total of 45 specimens (27 specimens for the nicotine and 18 specimens for the CSC-treated samples) were used and were selected randomly for each group. The control group consisted of 0 mg/ml of nicotine or CSC. The viability of C. albicans was measured using spiral plating on blood agar plates. The effect of nicotine and CSC concentrations on planktonic cells was were measured using a microplate reader. Metabolic activity of 24-hour-old established C. albicans biofilm exposed to nicotine and CSC for 24 hours in microtiter plates was determined using a 2,3-bis (2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-carboxanilide (XTT) reduction assay. RESULTS:The viability of C. albicans increased concomitant with increasing concentrations of CSC and nicotine, particularly at 0.5 and 2 mg/ml, respectively. Concentrations of CSC and nicotine above this resulted in an inhibitory effect on C. albicans viability. CSC and nicotine at 4 and 16 mg/ml, respectively, increased C. albicans biofilm metabolic activity. CONCLUSION:Nicotine and CSC up to certain concentrations caused increases in biofilm formation, metabolic activity, viability, and planktonic cell absorbance of C. albicans. This in vitro study demonstrates the effectiveness of tobacco on promoting the growth of C. albicans and suggests their potential contributing factor in C. albicans biofilm related infections in smokers.

译文

目的:吸烟者增加的假牙口腔炎主要由白色念珠菌引起。这项研究的主要目的是证明各种尼古丁和香烟烟雾冷凝物(CSC)的浓度对丙烯酸假牙材料上白念珠菌生物膜形成和代谢活性的影响。
材料与方法:C.使用白色念珠菌(ATCC菌株10231)。将标准义齿丙烯酸(PMMA)标本(共135个标本)与白色念珠菌一起孵育,并以不同浓度(0、0.25、0.5、1、2、4、8、16和32 mg / ml的尼古丁和CSC暴露) )和(0、0.25、0.5、1、2和4 mg / ml)。对于每个实验,每个尼古丁和CSC浓度使用3个样品,共使用45个样本(尼古丁为27个样本,CSC处理的样本为18个样本),并随机选择每组。对照组由0 mg / ml尼古丁或CSC组成。使用螺旋琼脂平板在血琼脂平板上测量白色念珠菌的生存力。使用酶标仪测量尼古丁和CSC浓度对浮游细胞的影响。使用2,3-双(2-甲氧基-4-硝基-5-硝基苯基)-2H-四唑鎓测定在微量滴定板中暴露于尼古丁和CSC中24小时的24小时建立的白色念珠菌生物膜的代谢活性-甲酰苯胺(XTT)还原测定。
结果:白色念珠菌的生存能力随着CSC和烟碱浓度的增加而增加,尤其是分别在0.5和2 mg / ml时。高于此浓度的CSC和烟碱会导致对白色念珠菌生存能力的抑制作用。 CSC和尼古丁分别以4和16 mg / ml的浓度增加白色念珠菌的生物膜代谢活性。
结论:高达一定浓度的尼古丁和CSC导致白色念珠菌的生物膜形成,代谢活性,活力和浮游细胞吸收增加。这项体外研究证明了烟草在促进白色念珠菌生长方面的有效性,并表明了烟草在吸烟者中白色念珠菌生物膜相关感染的潜在影响因素。

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