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鼻咽上皮细胞无时无刻不暴露和接触到共生微生物与病原微生物,机体依靠天然防御系统和抗原识别的适应性免疫反应系统来进行自我保护.慢性感染的重要毒力因素被认为是革兰氏阴性细菌细胞壁的主要成分脂多糖(LPS),对LPS的识别与信号传导是宿主细胞抵御革兰氏阴性细菌的关键.通过流式细胞术、RT-PCR等研究发现,5-8F细胞可与LPS相结合并产生反应,且其受LPS调节的机制是由于5-8F细胞中存在LPS受体分子如CD14、TLR4与MD2等的表达.同时应用免疫荧光、蛋白质印迹、荧光素酶报告系统等研究发现,5-8F细胞可受到LPS的诱导而活化TLR4的下游信号传导通路.5-8F细胞在LPS的诱导下,磷酸化NFκBp65的表达增加,并且使NFκBp65活化迁移至核内.研究还发现,LPS增加TNF-α全长启动子活性,同时LPS可使5-8F细胞中TNF-α的分泌增加,从而介导炎性因子的释放.因此,5-8F细胞可通过与LPS受体分子:CD14、TLR4及MD2与LPS相结合并反应,从而激活TLR4介导的NFκB信号通路,使炎性因子的释放增加,导致鼻咽部的炎症反应诱发鼻咽癌.
Nasopharyngeal epithelial cells are exposed all the time and come into contact with symbiotic microorganisms and pathogenic microorganisms, the body relies on the adaptive immune response system of natural defense system and antigen recognition to protect themselves.The important virulence factor of chronic infection is considered Gram-negative bacteria The main component of cell wall lipopolysaccharide (LPS), recognition and signal transduction LPS host cells against Gram-negative bacteria is the key.By flow cytometry, RT-PCR and other studies found that 5-8F cells with LPS phase And its mechanism of LPS regulation is due to the presence of LPS receptor molecules such as CD14, TLR4 and MD2 in 5-8F cells.Meanwhile, immunofluorescence, western blot, luciferase reporter system and other studies have found , 5-8F cells can be induced by LPS to activate the downstream signaling pathway of TLR4.5-8F cells under the LPS induced increased expression of phosphorylated NFκBp65 and NFκBp65 activation and migration to the nucleus.Studies also found that LPS Increase the activity of TNF-α full-length promoter, and at the same time LPS can increase the secretion of TNF-α in 5-8F cells and thus mediate the release of inflammatory cytokines. Therefore, 5-8F cells can differentiate into LPS- : CD14, TLR4 and MD2 combined and reacted with LPS, which activates TLR4 signaling pathway mediated by NFκB, so that increased release of inflammatory cytokines, leading to inflammation induced nasopharyngeal carcinoma of the nasopharynx.