Characterization of Innate Immune Responses of Human Endothelial Cells Induced byPorphyromonas gingivalisand Their Derived Outer Membrane Vesicles.
Atherosclerosis, a chronic inflammatory disease of the blood vessels, is one of the most common causes of morbidity and mortality world-wide. Involvement ofPorphyromonas gingivalisin atherosclerosis is supported by observations from epidemiological, clinical, immunological, and molecular studies. Previously we reported thatP. gingivalisvesicles have a much higher invasive efficiency than their originating cells. Here, we further compare the role ofP. gingivaliscells and their vesicles in expression of chemoattractant proteins including CXCL1, CXCL2, and CXCL8, and adhesive molecules such as E-selectin in human umbilical vein endothelial cells (HUVECs). BothP. gingivalis33277 cells and vesicles were able to up-regulate expression of these molecules, while the vesicles acted as more potent inducers of the inflammatory response associated with the development of atherosclerosis, consequently resulting in significant monocyte adhesion to a monolayer of HUVECs. Interestingly, we found that elevated expression of CXCL8 and E-selectin in endothelial cells induced byP. gingivaliscorrelated with the invasive ability ofP. gingivaliscells and vesicles. Non-invasive bacterial cells and vesicles had no effect on expression of these genes. This study highlights the potential risk ofP. gingivaliscells and vesicles in initiation of atherosclerosis and provides a potential target for the development of novel therapeutics against bacteria-associated atherosclerosis.
Oral Biology, School of Dentistry, Meharry Medical College Nashville, TN, USA.
Meng-Hsuan
MH
Ho
Department of Physiology, Meharry Medical College Nashville, TN, USA.
Zhong-Mao
ZM
Guo
Fisk University Nashville, TN, USA.
Julio
J
Chunga
Department of Biochemistry and Cancer Biology, Meharry Medical College Nashville, TN, USA.
J Shawn
JS
Goodwin
Oral Biology, School of Dentistry, Meharry Medical College Nashville, TN, USA.
Hua
H
Xie
D050197:Atherosclerosis / Q000276:immunology* / Q000382:microbiology*; D001425:Bacterial Outer Membrane Proteins / Q000378:metabolism; D001808:Blood Vessels; D002448:Cell Adhesion; D002478:Cells, Cultured; D054360:Chemokine CXCL1 / Q000096:biosynthesis / Q000235:genetics; D054426:Chemokine CXCL2 / Q000096:biosynthesis / Q000235:genetics; D019040:E-Selectin / Q000096:biosynthesis / Q000235:genetics; D042783:Endothelial Cells / Q000276:immunology* / Q000378:metabolism*; D005786:Gene Expression Regulation; D054884:Host-Pathogen Interactions; D061307:Human Umbilical Vein Endothelial Cells / Q000382:microbiology; D006801:Humans; D007113:Immunity, Innate; D016209:Interleukin-8 / Q000096:biosynthesis / Q000235:genetics; D009000:Monocytes / Q000378:metabolism; D016966:Porphyromonas gingivalis / Q000276:immunology* / Q000472:pathogenicity; D015854:Up-Regulation
D001425:Bacterial Outer Membrane Proteins; C475829:CXCL1 protein, human; C499706:CXCL2 protein, human; C508606:CXCL8 protein, human; D054360:Chemokine CXCL1; D054426:Chemokine CXCL2; D019040:E-Selectin; D016209:Interleukin-8; C546936:SELE protein, human
E-selectin; IL-8; P. gingivalis; atherosclerosis; outer membrane vesicles