牙龈卟啉单胞菌对肺部上皮细胞增殖及凋亡的影响

Effects of porphyromonas gingivalis on proliferation and apoptosis of pulmonary epithelial cells

目的探究牙龈卟啉单胞菌(porphyromonas gingivalis,Pg)对人支气管上皮细胞(16HBE)和人肺腺癌细胞(SPC-A-1)的增殖及凋亡的影响,揭示牙周致病菌感染造成肺炎的机制.方法建立Pg感染16HBE及SPC-A-1的体外模型,在感染后12、24、36、48 h检测Caspase-3酶的活性,分别采用ELISA和RT-PCR技术对白细胞介素(IL)-6、IL-8、STAT3、转化生长因子-β(TGF-β)、Bax、Survivn、Fas、FasL表达水平进行检测.结果牙龈卟啉单胞菌感染肺部上皮细胞后,24 h时细胞活力明显受到抑制(P<0.05),Caspase-3酶活性在12 h时明显增强(P<0.05).16HBE细胞的IL-6及IL-8均在12 h即有明显的增加(P<0.05);SPC-A-1细胞在24 h时IL-6及IL-8有明显的增加.2种肺上皮细胞在12 h时凋亡因子Bax、Fas、Fasl即显著性增加(P<0.05);16HBE细胞在48 h时增殖因子Bcl-2及TGF-β表达抑制显著(P<0.05);SPC-A-1细胞在36 h时增殖因子Bcl-2及TGF-β的表达显著受到抑制(P<0.05).结论牙龈卟啉单胞菌能够引起肺部上皮细胞的炎症反应,并促进促凋亡因子Bax、Fas、FasL及抑制促增殖因子Bcl-2、TGF-β的表达,从而导致肺炎的发生,造成肺部的损伤.

Objective To investigating the effect of porphyromonas gingivalis(Pg) on proliferation and apoptosis of human bronchial epithelial cells(16 HBE) and human lung adenocarcinoma cells(SPC-A-1), thus to reveal the mechanism of pneumonia caused by periodontal pathogen infection. Methods In vitro models of Pg infection with 16 HBE and SPC-A-1 were established. Caspase-3 activity were assessed 12 h, 24 h, 36 h and 48 h after infection. Expression levels of IL-6, IL-8, STAT3, TGF-β, Bax, Survivn, Fas and FasL were assessed by ELISA and RT-PCR at each time point. Results After Pg infection, cell activity of pulmonary epithelial cells was significantly inhibited at 24 h(P<0.05), and Caspase-3 activity was significantly enhanced at 12 h(P<0.05). Both IL-6 and IL-8 in 16 HBE cells were significantly increased at 12 h(P<0.05). SPC-A-1 cells showed significant increases in IL-6 and IL-8 at 24 h. The apoptotic factors Bax, Fas and Fasl were significantly increased in the two types of lung epithelial cells at 12 h(P<0.05). The proliferation factor Bcl-2 and TGF-β were significantly inhibited in 16 HBE cells at 48 h(P<0.05). The expression of proliferation factor Bcl-2 and TGF-β present in SPC-A-1 cells was significantly inhibited at 36 h(P<0.05). Conclusion Pg can induce the inflammatory response of pulmonary epithelial cells, promote the expression of pro-apoptotic factors Bax, Fas, FasL and inhibit the expression of pro-proliferative factors Bcl-2 and TGF-β, thus leading to the occurrence of pneumonia and the damage to the lungs.