title: Expression of RANKL and proliferation abilities of cultured human middle ear cholesteatoma epithelial cells.
abstract: One of the most distinct characteristics of middle ear cholesteatomas is their capacity for bone destruction during the growth process. In this study, we examined the relationship between inflammatory mechanisms and both bone absorption and the proliferation of epithelial cholesteatoma cells. Cultured cholesteatoma epithelial cells were stimulated by lipopolysaccharide (LPS) and dexamethasone (Dex). We found that the expression of receptor activator of NF-kappaB ligand (RANKL) and Ki-67 in cultured cholesteatoma cells was increased by LPS stimulation, indicating that LPS promotes not only bone destruction but also the proliferative activities of these cells. The constitutive expression of RANKL and Ki-67 and the production of IL-6 and IL-8 were significantly inhibited by Dex treatment. Further, Dex significantly suppressed the stimulatory effects of LPS on RANKL and Ki-67 expression and on IL-6 and IL-8 production. Based on results so far, Dex likely exerts a beneficial action against acute inflammation. However, further studies might be required to assess its clinical features.
authors.affiliation: Department of Otorhinolaryngology, Head and Neck Surgery, Graduate School of Biomedical Sciences, Hiroshima University, Japan. mymarin@mri.biglobe.ne.jp
authors.forename: Marin
authors.initials: M
authors.lastname: Miyasato
authors.forename: Sachio
authors.initials: S
authors.lastname: Takeno
authors.forename: Katsuhiro
authors.initials: K
authors.lastname: Hirakawa
mesh_terms: D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D001862:Bone Resorption / Q000378:metabolism / Q000473:pathology; D049109:Cell Proliferation / Q000187:drug effects; D002478:Cells, Cultured; D018424:Cholesteatoma, Middle Ear / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D003907:Dexamethasone / Q000494:pharmacology; D004432:Ear, Middle / Q000187:drug effects / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D004847:Epithelial Cells / Q000187:drug effects / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D018836:Inflammation Mediators / Q000378:metabolism*; D015850:Interleukin-6 / Q000378:metabolism; D016209:Interleukin-8 / Q000378:metabolism; D019394:Ki-67 Antigen / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology; D053245:RANK Ligand / Q000378:metabolism*
chemical_list: D000893:Anti-Inflammatory Agents; C508606:CXCL8 protein, human; C508600:IL6 protein, human; D018836:Inflammation Mediators; D015850:Interleukin-6; D016209:Interleukin-8; D019394:Ki-67 Antigen; D008070:Lipopolysaccharides; D053245:RANK Ligand; C505688:TNFSF11 protein, human; D003907:Dexamethasone