Wallace Daniel F, Subramaniam V Nathan
Membrane Transport Laboratory, QIMR Berghofer Medical Research Institute, Brisbane, Queensland 4006, Australia and School of Medicine, University of Queensland, Brisbane, Queensland 4006, Australia.
Membrane Transport Laboratory, QIMR Berghofer Medical Research Institute, Brisbane, Queensland 4006, Australia and School of Medicine, University of Queensland, Brisbane, Queensland 4006, Australia
Int Immunol. 2015 Jun;27(6):281-7. doi: 10.1093/intimm/dxu144. Epub 2015 Jan 7.
The anaemia of chronic disease (ACD) results from inflammation-mediated up-regulation of the iron regulatory hormone hepcidin, with the consequent sequestration of iron limiting its availability for erythropoiesis. The inflammatory cytokine IL-6, a regulator of hepcidin, has been implicated in this process. Recent in vivo and in vitro studies indicate that IL-22 is also able to stimulate hepcidin expression. We aimed to determine if IL-22 had a role in causing the hypoferremia associated with the inflammatory response. Wild-type and Il22-knockout mice were subjected to an acute inflammatory stimulus via administration of LPS and the response of hepcidin and iron homeostasis was analysed. In the absence of IL-22, there was a response of hepcidin, resulting in a reduction in serum iron levels. However, the hypoferremic response to LPS was slightly blunted in mice lacking IL-22, suggesting that, during LPS-mediated inflammation, IL-22 may play a minor role in mediating the hypoferremic response. These results may have implications for the treatment and management of the ACD.
慢性病贫血（ACD）是由炎症介导的铁调节激素铁调素上调所致，铁随之被隔离，限制了其在红细胞生成中的可用性。炎性细胞因子白细胞介素-6（IL-6）作为铁调素的调节因子，参与了这一过程。最近的体内和体外研究表明，IL-22也能够刺激铁调素的表达。我们旨在确定IL-22是否在引发与炎症反应相关的低铁血症中起作用。通过给予脂多糖（LPS）对野生型和IL-22基因敲除小鼠进行急性炎症刺激，并分析铁调素的反应和铁稳态。在缺乏IL-22的情况下，铁调素会产生反应，导致血清铁水平降低。然而，在缺乏IL-22的小鼠中，对LPS的低铁血症反应略有减弱，这表明在LPS介导的炎症过程中，IL-22可能在介导低铁血症反应中起次要作用。这些结果可能对ACD的治疗和管理具有启示意义。
