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.