title: A glycoprotein from Spirometra erinaceieuropaei plerocercoids suppresses osteoclastogenesis and proinflammatory cytokine gene expression.
abstract: Various parasites modify the immune-reactions of the host. We have previously shown that crude excretory/secretory (ES) products from plerocercoids of Spirometra erinaceieuropaei, the plerocercoids of which cause sparganosis in humans, suppress the expression of tumor necrosis factor (TNF)-alpha and IL-1beta in lipopolysaccharide (LPS)-stimulated macrophages. As osteoclasts are cells of the monocyte/macrophage lineage, we hypothesised that ES products might suppress receptor activator of nuclear factor kappaB ligand-induced osteoclastogenesis. Crude ES products from plerocercoids suppressed osteoclastogenesis, judged by tartrate-resistant acid phosphatase (TRAP)-positive multinuclear cell counting, and the mature osteoclast-specific gene expression (calcitonin receptor and TRAP). Second, we purified the inhibitory factor for osteoclastogenesis from the crude ES products. The factor was a trypsin-sensitive glycoprotein and had a relative molecular mass of 90 kDa. The glycoprotein, plerocercoid-immunosuppressive factor, from crude ES products could suppress the gene expression of TNF-alpha, IL-1beta and NO synthesis in LPS-stimulated RAW264.7 macrophages.
authors.affiliation: Division of Molecular Medical Zoology, Department of Microbiology and Pathology, Faculty of Medicine, Tottori University, 86 Nishi-cho, Tottori, Yonago 683-8503, Japan.
authors.forename: Yuriko
authors.initials: Y
authors.lastname: Kina
authors.forename: Soji
authors.initials: S
authors.lastname: Fukumoto
authors.forename: Kazutoyo
authors.initials: K
authors.lastname: Miura
authors.forename: Sayuri
authors.initials: S
authors.lastname: Tademoto
authors.forename: Kozue
authors.initials: K
authors.lastname: Nunomura
authors.forename: Paramasari
authors.initials: P
authors.lastname: Dirgahayu
authors.forename: Kazumitsu
authors.initials: K
authors.lastname: Hirai
mesh_terms: D000818:Animals; D001685:Biological Factors / Q000494:pharmacology; D001854:Bone Marrow Cells / Q000166:cytology / Q000187:drug effects; D002352:Carrier Proteins / Q000037:antagonists & inhibitors / Q000502:physiology; D002454:Cell Differentiation / Q000187:drug effects; D002460:Cell Line; D016207:Cytokines / Q000096:biosynthesis* / Q000235:genetics; D005786:Gene Expression Regulation / Q000187:drug effects; D006023:Glycoproteins / Q000302:isolation & purification / Q000494:pharmacology*; D015801:Helminth Proteins / Q000302:isolation & purification / Q000494:pharmacology*; D007375:Interleukin-1 / Q000096:biosynthesis / Q000235:genetics; D008070:Lipopolysaccharides / Q000276:immunology; D008562:Membrane Glycoproteins / Q000037:antagonists & inhibitors / Q000502:physiology; D051379:Mice; D010010:Osteoclasts / Q000187:drug effects* / Q000502:physiology; D053245:RANK Ligand; D053246:Receptor Activator of Nuclear Factor-kappa B; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D013146:Spirometra / Q000737:chemistry*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis / Q000235:genetics
chemical_list: D001685:Biological Factors; D002352:Carrier Proteins; D016207:Cytokines; D006023:Glycoproteins; D015801:Helminth Proteins; D007375:Interleukin-1; D008070:Lipopolysaccharides; D008562:Membrane Glycoproteins; D053245:RANK Ligand; D053246:Receptor Activator of Nuclear Factor-kappa B; C505687:Tnfrsf11a protein, mouse; C505689:Tnfsf11 protein, mouse; D014409:Tumor Necrosis Factor-alpha