CAJ | 학술논문

目的观察牙龈卟啉单胞菌(Porphyromonas gigivalis,Pg)感染单核细胞后是否增加单核细胞对人脐静脉内皮细胞(human umbilical vein endothelial cell,HUVEC)的黏附并探讨其分子机制,为从牙周病的角度预防动脉粥样硬化的发生提供新的研究思路.方法应用厌氧罐培养Pg,以感染复数为1∶100感染人单核细胞株THP-1.感染0(对照组)、8和24h后与HUVEC共培养1h,去除未黏附的THP-1后观察THP-1对HUVEC的黏附,再培养23 h后用酶联免疫吸附测定法检测相应细胞因子的表达及黏附分子的变化.结果 Pg感染24h后,THP-1对HUVEC的黏附较对照组提高了13.8％～35.2％ (P =0.006);细胞间黏附分子1的表达量[(164.9±9.1) ng/L]显著高于对照组[(132.5±7.7) ng/L] (P =0.005);单核细胞趋化蛋白1的分泌量[(221.0±4.9)ng/L]显著高于对照组[(183.2±3.1)ng/L](P=0.012);细胞分泌白细胞介素8的量[(787.2±10.3) ng/L]亦显著高于对照组[(587.2±5.1)ng/L] (P=0.002).结论 Pg感染促进单核细胞与HUVEC的黏附;Pg感染可能是动脉粥样硬化发生的危险因素.
목적 관찰아간계람단포균(Porphyromonas gigivalis,Pg)감염단핵세포후시부증가단핵세포대인제정맥내피세포(human umbilical vein endothelial cell,HUVEC)적점부병탐토기분자궤제,위종아주병적각도예방동맥죽양경화적발생제공신적연구사로.방법 응용염양관배양Pg,이감염복수위1∶100감염인단핵세포주THP-1.감염0(대조조)、8화24h후여HUVEC공배양1h,거제미점부적THP-1후관찰THP-1대HUVEC적점부,재배양23 h후용매련면역흡부측정법검측상응세포인자적표체급점부분자적변화.결과 Pg감염24h후,THP-1대HUVEC적점부교대조조제고료13.8％～35.2％ (P =0.006);세포간점부분자1적표체량[(164.9±9.1) ng/L]현저고우대조조[(132.5±7.7) ng/L] (P =0.005);단핵세포추화단백1적분비량[(221.0±4.9)ng/L]현저고우대조조[(183.2±3.1)ng/L](P=0.012);세포분비백세포개소8적량[(787.2±10.3) ng/L]역현저고우대조조[(587.2±5.1)ng/L] (P=0.002).결론 Pg감염촉진단핵세포여HUVEC적점부;Pg감염가능시동맥죽양경화발생적위험인소.
Objective To observe if Porphyromonas gingivalis (Pg) infection could enhance the adhesion of human monocytic cell line (THP-1) to human umbihcal vein endothelial cells (HUVEC).Methods PgATCC33277 was cultured in anaerobic jar,and THP-1 was infected with various concentrations of PgATCC33277 at multiplicity of infection(MOI) of 1:100 for 8 and 24 hours,respectively.Mter removal of the free Pg,THP-1 cells were cocultured with HUVEC for 1 hour to observe the adhesion of THP-1 to HUVEC.HUVEC with adhesive THP-1 cells were co-cultured for additional 23 hours.The medium and cells were separately collected.The expression of related chemotactic cytokine [monocyte chemotactic protein 1 (MCP-1) and interleukin 8 (IL-8)] and intercellular adhesion molecule-1 (ICAM-1) were detected with enzyme-linked immunosorbent assay.Results The adhesion of THP-1 to HUVEC was enhanced (13.8％-35.2％,P=0.006) and the expression of ICAM-1 of HUVEC was increased from (132.5 ±7.7) to (164.9 ±9.1) ng/L (P=0.005) after infection for 24 hours by Pg.Both of the secreted MCP-I and IL-8 elevated after infection of Pg for 24 hours from (183.2 ± 3.1) to (221.0 ± 4.9) ng/L (P =0.012) and from (587.2 ±5.1) to (787.2 ± 10.3) ng/L (P =0.002),respectively.Conclusions Pg could enhance the adhesion of monocytes to endothelial cells and stimulate the inflammation,suggesting that Pg infection may be one of the risk factors in promoting the development of atherosclerosis.