Audiology & neuro-otology · 2012
Effect of angiotensin II on inflammation pathways in human primary bone cell cultures in otosclerosis.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Rudić Milan, Nguyen Christine, Nguyen Yann, Milković Lidija, Zarković Neven, Sterkers Olivier, Ferrary Evelyne, Bozorg Grayeli Alexis
Аннотация
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.
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.