title: [Molecular mechanism involved in adhesion of monocytes to endothelial cells induced by nicotine and Porphyromonas gingivalis-LPS].
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 U937 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 endothelial cells (HUVECs), the expressions of monocyte chemoattractant protein CCL-8 and adhesion molecules 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 U937 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 U937 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 combination 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.
  
  
  CONCLUSIONS
  P.g-LPS in combination 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/VLA4α and OX40/OX40L interactions, which could be involved in the initiation and development of atherosclerosis.
authors.affiliation: Central Laboratory, Peking University School and Hospital of Stomatology, Beijing 100081, China.
authors.forename: Yi-xiang
authors.initials: YX
authors.lastname: Wang
authors.affiliation: Department of General Dentistry II, Peking University School and Hospital of Stomatology, Beijing 100081, China.
authors.forename: Na
authors.initials: N
authors.lastname: An
authors.affiliation: Department of Periodontology, Peking University School and Hospital of Stomatology, Beijing 100081, China.
authors.forename: Xiang-ying
authors.initials: XY
authors.lastname: Ouyang
mesh_terms: D002448:Cell Adhesion; D015815:Cell Adhesion Molecules / Q000378:metabolism; D002460:Cell Line; D061307:Human Umbilical Vein Endothelial Cells / Q000166:cytology*; D006801:Humans; D015850:Interleukin-6 / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology*; D009000:Monocytes / Q000166:cytology* / Q000187:drug effects; D009538:Nicotine / Q000494:pharmacology*; D016966:Porphyromonas gingivalis / Q000166:cytology; D015854:Up-Regulation
chemical_list: D015815:Cell Adhesion Molecules; C508600:IL6 protein, human; D015850:Interleukin-6; D008070:Lipopolysaccharides; D009538:Nicotine