title: Inductive effect of Porphyromonas gingivalis fimbriae on differentiation of human monocytic tumor cell line U937.
abstract: This study used the human monocytic tumor cell line U937 to examine whether Porphyromonas gingivalis fimbriae induce differentiation of monocyte/macrophage progenitors. When the progenitor cells were incubated with P. gingivalis fimbriae, the incubation resulted in increased Fc rosette formation and increased CD11b production by the cells. The presence of a protein kinase C inhibitor, H7 or calphostin C, in the medium eliminated the stimulatory effects of P. gingivalis fimbriae on Fc rosette formation. Furthermore, CD11b expression was inhibited by calphostin C. In contrast, HA1004 , an inhibitor of cyclic nucleotide-dependent protein kinase, had no effect on P. gingivalis fimbriae-induced Fc rosette formation or CD11b expression. These results demonstrate that P. gingivalis fimbriae are a potent inducer of the differentiation of the monocyte/macrophage tumor cell line U937, most probably via cyclic nucleotide-independent protein kinase C.
authors.affiliation: Department of Preventive Dentistry, Health Sciences University of Hokkaido, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Hirose
authors.forename: E
authors.initials: E
authors.lastname: Isogai
authors.forename: H
authors.initials: H
authors.lastname: Mizugai
authors.forename: H
authors.initials: H
authors.lastname: Miura
authors.forename: I
authors.initials: I
authors.lastname: Ueda
mesh_terms: D019307:1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; D000942:Antigens, Bacterial / Q000276:immunology; D015703:Antigens, CD / Q000276:immunology; D002454:Cell Differentiation / Q000502:physiology; D004791:Enzyme Inhibitors / Q000378:metabolism; D010861:Fimbriae, Bacterial / Q000276:immunology / Q000502:physiology*; D006412:Hematopoietic Stem Cells / Q000382:microbiology* / Q000502:physiology; D006801:Humans; D007375:Interleukin-1 / Q000096:biosynthesis / Q000502:physiology; D007546:Isoquinolines / Q000378:metabolism; D016177:Macrophage-1 Antigen / Q000096:biosynthesis; D008264:Macrophages / Q000382:microbiology / Q000502:physiology; D009000:Monocytes / Q000382:microbiology / Q000502:physiology; D009281:Naphthalenes / Q000378:metabolism; D014411:Neoplastic Stem Cells / Q000382:microbiology* / Q000502:physiology; D010879:Piperazines / Q000378:metabolism; D016966:Porphyromonas gingivalis / Q000276:immunology / Q000502:physiology* / Q000648:ultrastructure; D011493:Protein Kinase C / Q000037:antagonists & inhibitors / Q000378:metabolism; D011961:Receptors, Fc; D012397:Rosette Formation; D015290:Second Messenger Systems; D015398:Signal Transduction; D013449:Sulfonamides; D014407:Tumor Cells, Cultured
chemical_list: D000942:Antigens, Bacterial; D015703:Antigens, CD; D004791:Enzyme Inhibitors; D007375:Interleukin-1; D007546:Isoquinolines; D016177:Macrophage-1 Antigen; D009281:Naphthalenes; D010879:Piperazines; D011961:Receptors, Fc; D013449:Sulfonamides; D019307:1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; C043204:N-(2-guanidinoethyl)-5-isoquinolinesulfonamide; D011493:Protein Kinase C; C058819:calphostin C