Koening Curry L, Miller Jennifer C, Nelson Jenifer M, Ward Diane M, Kushner James P, Bockenstedt Linda K, Weis Janis J, Kaplan Jerry, De Domenico Ivana
Division of Rheumatology, Department of Internal Medicine, University of Utah, Salt Lake City, UT 84132, USA.
Blood. 2009 Aug 27;114(9):1913-8. doi: 10.1182/blood-2009-03-209577. Epub 2009 Jul 8.
Hepcidin is the major regulator of systemic iron homeostasis in mammals. Hepcidin is produced mainly by the liver and is increased by inflammation, leading to hypoferremia. We measured serum levels of bioactive hepcidin and its effects on serum iron levels in mice infected with Borrelia burgdorferi. Bioactive hepcidin was elevated in the serum of mice resulting in hypoferremia. Infected mice produced hepcidin in both liver and spleen. Both intact and sonicated B burgdorferi induced hepcidin expression in cultured mouse bone marrrow macrophages. Hepcidin production by cultured macrophages represents a primary transcriptional response stimulated by B burgdorferi and not a secondary consequence of cytokine elaboration. Hepcidin expression induced by B burgdorferi was mediated primarily by activation of Toll-like receptor 2.
铁调素是哺乳动物体内系统性铁稳态的主要调节因子。铁调素主要由肝脏产生，并因炎症而增加，导致低铁血症。我们检测了感染伯氏疏螺旋体的小鼠血清中生物活性铁调素的水平及其对血清铁水平的影响。感染小鼠血清中的生物活性铁调素升高，导致低铁血症。感染小鼠的肝脏和脾脏均产生铁调素。完整的和超声处理的伯氏疏螺旋体均可诱导培养的小鼠骨髓巨噬细胞中铁调素的表达。培养的巨噬细胞产生铁调素代表了伯氏疏螺旋体刺激的一种主要转录反应，而非细胞因子分泌的次要结果。伯氏疏螺旋体诱导的铁调素表达主要由Toll样受体2的激活介导。
