Molecular mechanism involved in adhesion of monocytes to endothelial cells induced by nicotine and Porphyromonas gingivalis-LPS
10.3969/j.issn.1671-167X.2015.05.015
- VernacularTitle:尼古丁和牙龈卟啉单胞菌脂多糖影响单核细胞黏附血管内皮细胞的分子机制
- Author:
Yixiang WANG
;
Na AN
;
Xiangying OUYANG
- Publication Type:Journal Article
- Keywords:
Nicotine;
Porphyromonas gingivalis;
Atherosclerosis;
Cell adhesion molecules
- From:
Journal of Peking University(Health Sciences)
2015;(5):809-813
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate molecular mechanism involved in nicotine in combination with Porphyromonas gingivalis ( P.g ) caused monocyte-endothelial cell adhesion .Methods: The effect of nicotine, P.g-lipopolysaccharide (P.g-LPS) and their combination on the proliferation of U 937 cells was determined by CCK-8 method .Interleukin-6 ( IL-6 ) expression was investigated by Real-time PCR after U937 cells were treated with nicotine , P.g-LPS and their combination .In human umbilical vein endothe-lial cells ( HUVECs ) , the expressions of monocyte chemoattractant protein CCL-8 and adhesion mole-cules including vascular cell adhesion molecule 1 ( Vcam-1 ) , very late antigen 4 alpha ( VLA4α) , tumor necrosis factor receptor superfamily member 4 ( OX40) and OX40 ligand ( OX40L) were detected by Real-time PCR or Western blotting assays after HUVEC cells were treated with nicotine , P.g-LPS and their combination .Adhesion of monocytes to endothelial cells was detected after the HUVECs and U 937 cells were stimulated with nicotine , P.g-LPS and their combination, respectively.Results:P.g-LPS did not affect the proliferative ability of nicotine in U 937 cells.However, the ability of P.g-LPS induced IL-6 expression was inhibited by 100 μmol/L nicotine in U937 cells.In HUVECs, the expressions of CCL-8, Vcam-1, VLA4α, OX40 and OX40L were significantly up-regulated by nicotine and P.g-LPS combi-nation compared with nicotine alone , P.g-LPS alone and the untreated control .Adhesion of monocytes to HUVECs results showed that the two types of cells treated with nicotine in combination with P.g-LPS could markedly increase the adhesion ability of monocytes to HUVECs .Conclusion:P.g-LPS in combi-nation with nicotine could recruit monocytes to endothelial lesion through up-regulation of CCL-8, and promote adhesion of monocytes to endothelial cells through enhancement of Vcam -1/VLA4αand OX40/OX40L interactions, which could be involved in the initiation and development of atherosclerosis .
