title: Endothelial Cell Response to Fusobacterium nucleatum.
abstract: Vascular response is an essential aspect of an effective immune response to periodontal disease pathogens, as new blood vessel formation contributes to wound healing and inflammation. Gaining a greater understanding of the factors that affect vascular response may then contribute to future breakthroughs in dental medicine. In this study, we have characterized the endothelial cell response to the common bacterium Fusobacterium nucleatum, an important bridging species that facilitates the activity of late colonizers of the dental biofilm. Endothelial cells were infected with Fusobacterium nucleatum (strain 25586) for periods of 4, 12, 24, or 48 h. Cell proliferation and tube formation were analyzed, and expression of adhesion molecules (CD31 and CD34) and vascular endothelial growth factor (VEGF) receptors 1 and 2 was measured by fluorescence-activated cell sorter (FACS) analysis. Data indicate that F. nucleatum impaired endothelial cell proliferation and tube formation. The findings suggest that the modified endothelial cell response acts as a mechanism promoting the pathogenic progression of periodontal diseases and may potentially suggest the involvement of periodontopathogens in systemic diseases associated with periodontal inflammation.
authors.affiliation: Forsyth Institute, Cambridge, Massachusetts, USA.|Ponta Grossa State University, Ponta Grossa, PR, Brazil.
authors.forename: Reila Tainá
authors.initials: RT
authors.lastname: Mendes
authors.affiliation: Forsyth Institute, Cambridge, Massachusetts, USA.
authors.forename: Daniel
authors.initials: D
authors.lastname: Nguyen
authors.affiliation: Forsyth Institute, Cambridge, Massachusetts, USA.
authors.forename: Danielle
authors.initials: D
authors.lastname: Stephens
authors.affiliation: Forsyth Institute, Cambridge, Massachusetts, USA.|Istanbul Aydin University, Istanbul, Turkey.
authors.forename: Ferda
authors.initials: F
authors.lastname: Pamuk
authors.affiliation: Ponta Grossa State University, Ponta Grossa, PR, Brazil.
authors.forename: Daniel
authors.initials: D
authors.lastname: Fernandes
authors.affiliation: Forsyth Institute, Cambridge, Massachusetts, USA.
authors.forename: Thomas E
authors.initials: TE
authors.lastname: Van Dyke
authors.affiliation: Forsyth Institute, Cambridge, Massachusetts, USA akantarci@forsyth.org.
authors.forename: Alpdogan
authors.initials: A
authors.lastname: Kantarci
mesh_terms: D015415:Biomarkers; D015815:Cell Adhesion Molecules / Q000235:genetics / Q000378:metabolism; D049109:Cell Proliferation; D016207:Cytokines / Q000378:metabolism; D042783:Endothelial Cells / Q000378:metabolism* / Q000382:microbiology*; D016967:Fusobacterium nucleatum / Q000502:physiology*; D015870:Gene Expression; D061307:Human Umbilical Vein Endothelial Cells; D006801:Humans; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000235:genetics / Q000378:metabolism; D018836:Inflammation Mediators / Q000378:metabolism; D018919:Neovascularization, Physiologic; D009569:Nitric Oxide / Q000096:biosynthesis; D040262:Receptors, Vascular Endothelial Growth Factor / Q000378:metabolism; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
chemical_list: D015415:Biomarkers; D015815:Cell Adhesion Molecules; D016207:Cytokines; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D018836:Inflammation Mediators; D042461:Vascular Endothelial Growth Factor A; D009569:Nitric Oxide; D040262:Receptors, Vascular Endothelial Growth Factor