Effect of Angiotensin II on Inflammation Pathways in Human Primary Bone Cell Cultures in Otosclerosis

Introduction: The aim of this study was to assess the expression and production of inflammation mediators in basal condition and after angiotensin II (AngII) in otosclerosis. Materials and Methods: Human stapedial cell cultures (6 otosclerosis and 6 controls) were incubated with AngII (10 –7 M, 24 h) or vehicle. Cytokines and their mRNA expression were assessed by antibody and cDNA arrays. Results: In basal conditions, otosclerotic cultures produced higher amounts of interleukin (IL)-1β and interferon-inducible protein 10, and smaller amounts of tissue inhibitor of metalloproteinase 2. AngII promoted inflammation by increasing interferon γ and IL-10, and by decreasing macrophage inflammatory protein 1α and soluble tumor necrosis factor receptor II. Conclusions: Otosclerotic cultures produced higher proinflammatory cytokines in basal condition. AngII appeared to promote inflammation via these mediators in otosclerosis.