Porphyromonas gingivalis infection enhanced the adhesion of monocytes to endothelial.
- Author:
Caixia ZHANG
1
;
Jie SONG
1
;
Jingjing LI
1
;
Xin GAO
1
;
Weibin SUN
1
;
Kuanyu LI
2
Author Information
- Publication Type:Journal Article
- MeSH: Bacteroidaceae Infections; metabolism; Cell Line; Cells, Cultured; Chemokine CCL2; biosynthesis; Coculture Techniques; Endothelial Cells; Human Umbilical Vein Endothelial Cells; Humans; Inflammation; Intercellular Adhesion Molecule-1; biosynthesis; Interleukin-8; biosynthesis; Monocytes; Porphyromonas gingivalis; pathogenicity; Umbilical Veins
- From: Chinese Journal of Stomatology 2014;49(3):151-154
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe if Porphyromonas gingivalis (Pg) infection could enhance the adhesion of human monocytic cell line (THP-1) to human umbilical vein endothelial cells (HUVEC).
METHODSPgATCC33277 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. After 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.
RESULTSThe 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-1 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.
CONCLUSIONSPg 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.