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机构地区:[1]中国医科大学口腔医学院.中国医科大学附属口腔医院牙周病科,辽宁沈阳110002
出 处:《口腔医学研究》2016年第3期211-215,共5页Journal of Oral Science Research
基 金:国家自然科学基金资助项目(编号:81271153和81470745)
摘 要:目的:通过研究牙龈卟啉单胞菌(Porphyromonasgingivalis,P.gingivalis)和具核梭杆菌(Fusobacteriumnucleatum,F.nucleatum)感染对KB细胞的细胞周期和炎症因子分泌的调控,初步探讨牙周细菌感染对口腔鳞状细胞癌进展和炎症反应的影响。方法:建立P.gingivalis和F.nucleatum单独或联合感染KB细胞模型,透射电镜观察细菌感染细胞情况,流式细胞术检测细胞周期变化,酶联免疫法检测IL-6和IL-8蛋白分泌水平。结果:P.gingivalis联合F.nucleatum感染KB细胞8h抑制细胞周期进程,感染24h后加速细胞周期进程;P.gingivalis联合F.nucleatum感染促进KB细胞分泌IL-6和IL-8,并且有时间和F.nucleatum浓度依赖性。结论:牙周致病菌之间的联合作用更能促进口腔鳞状细胞癌的发展及免疫炎症反应。Objective:To investigate the effects of P.gingivalis/F.nucleatumon the cell cycle and cytokines production of KB cells.Methods:In vitro models were established with KB cells co-cultured with P.gingivalis/F.nucleatumeither alone or in combination.Transmission electron microscopy was used to observed invasive ability,the change of cell cycle of KB cells was detected by flow cytometry,and the production of interleukin-6(IL-6)and interleukin-8(IL-8)was analyzed by enzyme-linked immunoadsordent assay.Results:Eight-hour co-infection with P.gingivalis/F.nucleatumslowed the cell cycle of KB cells,while eight-hour co-infection accelerated the cell cycle.The production of IL-6and IL-8was significantly up-regulated after co-infection with P.gingivalis/F.nucleatumin a time dependent and F.nucleatum density related manner.Conclusion:Combination of oral pathogens can stimulate tumorigenesis and inflammation response in OSCC.
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