CAJ | 학술논문

目的观察牙龈卟啉单胞菌(P.gingivalis)W83和ATCC33277株侵入在单核细胞对内皮细胞黏附作用中的影响,及在内皮细胞细胞间黏附分子l(ICAM-1)转录和翻译中的作用. 方法建立体外P.gingivalis侵入内皮细胞模型,孟加拉玫瑰红活细胞染色法测定P.gingivalis侵入前后单核细胞对内皮细胞黏附的变化;RT-PCR和mRNA比色定量法检测内皮细胞ICAM-1基因表达;West-ern blot检测ICAM-1蛋白水平的变化. 结果 P.gingivalis W83和ATCC33277株侵入可增加单核细胞对内皮细胞的黏附,抗ICAM-1抗体部分抑制P.gingivalis侵入介导的单核细胞对内皮细胞黏附增加;P.gingivalis侵入上调内皮细胞ICAM-l基因和蛋白的表达,W83诱导单核细胞对内皮细胞黏附增强及内皮细胞ICAM-1表达的能力强于ATCC33277. 结论 ICAM-1在P.gingivalis介导的单核细胞对内皮细胞黏附增强过程中起部分作用,P.gingivalis侵入内皮细胞诱导ICAM-1表达可能是其诱发动脉粥样硬化疾病的机制之一.
목적 관찰아간계람단포균(P.gingivalis)W83화ATCC33277주침입재단핵세포대내피세포점부작용중적영향,급재내피세포세포간점부분자l(ICAM-1)전록화번역중적작용. 방법 건입체외P.gingivalis침입내피세포모형,맹가랍매괴홍활세포염색법측정P.gingivalis침입전후단핵세포대내피세포점부적변화;RT-PCR화mRNA비색정량법검측내피세포ICAM-1기인표체;West-ern blot검측ICAM-1단백수평적변화. 결과 P.gingivalis W83화ATCC33277주침입가증가단핵세포대내피세포적점부,항ICAM-1항체부분억제P.gingivalis침입개도적단핵세포대내피세포점부증가;P.gingivalis침입상조내피세포ICAM-l기인화단백적표체,W83유도단핵세포대내피세포점부증강급내피세포ICAM-1표체적능력강우ATCC33277. 결론 ICAM-1재P.gingivalis개도적단핵세포대내피세포점부증강과정중기부분작용,P.gingivalis침입내피세포유도ICAM-1표체가능시기유발동맥죽양경화질병적궤제지일.
Objective To observe the role of Porphyromonas P.gingivalis(P.gingivalis)invasion on monocyte adhesion to endothelium and its effect on the intercellular adhesion molecule-1(ICAM-1)produc-tion in endothelial cells.Methods A cell culture model of human umbilical vein endothelial cells (HUVEC) Was used in vitro.The adhesion of monocytes to HUVEC was detected by Rose Bengal staining with or without P.gingivalis invasion.The ICAM-1 mRNA expression in HUVEC Was determined by RT-PCR or quantikine mRNA colorimetric quantification kits.Cell surface protein of ICAM-1 in HUVEC was de-termined by Western blot with or without P.gingivalis invasion.Results The adhesion of monocyte to endo-thelium and expression of ICAM-1(both at mRNA and protein level)were found to be enhanced by P.gingi-valis invasion.Pretreatment of HUVEC with anti-ICAM-l antibody partly abolished the increase in monocyte adhesion to endothelium.Furthermore.the effect of virulent strain W83 was stronger than that of avirulent strain ATCC33277.Condusion P.gingivalis plays an important role in monocyte-endothelium adhesion partly through up regulation of ICAM-1,which may be one of the pathologic mechallisms in atherosclerosis.