Rudić Milan, Nguyen Christine, Nguyen Yann, Milković Lidija, Zarković Neven, Sterkers Olivier, Ferrary Evelyne, Bozorg Grayeli Alexis
Inserm, UMRS, Paris-Diderot University, France.
Audiol Neurootol. 2012;17(3):169-78. doi: 10.1159/000335098. Epub 2012 Jan 25.
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.
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.
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.
Otosclerotic cultures produced higher proinflammatory cytokines in basal condition. AngII appeared to promote inflammation via these mediators in otosclerosis.
本研究的目的是评估耳硬化症患者在基础状态下以及血管紧张素II（AngII）作用后炎症介质的表达和产生情况。
将人镫骨细胞培养物（6例耳硬化症患者和6例对照）与AngII（10⁻⁷M，24小时）或溶剂孵育。通过抗体和cDNA阵列评估细胞因子及其mRNA表达。
在基础状态下，耳硬化症培养物产生较高量的白细胞介素（IL）-1β和干扰素诱导蛋白10，以及较少量的金属蛋白酶组织抑制剂2。AngII通过增加干扰素γ和IL-10，以及减少巨噬细胞炎性蛋白1α和可溶性肿瘤坏死因子受体II来促进炎症。
耳硬化症培养物在基础状态下产生较高的促炎细胞因子。AngII似乎通过这些介质在耳硬化症中促进炎症。
