• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cytokine >Elevated levels of Interleukin (IL)-33 induce bone pathology but absence of IL-33 does not negatively impact normal bone homeostasis
【24h】

Elevated levels of Interleukin (IL)-33 induce bone pathology but absence of IL-33 does not negatively impact normal bone homeostasis

机译：高水平的白介素（IL）-33会诱发骨病变，但是IL-33的缺乏不会对正常的骨稳态产生负面影响

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Interleukin (IL)-33 is a member of the IL-1 family. IL-33 effects are mediated through its receptor, ST2 and IL-1RAcP, and its signaling induces the production of a number of pro-inflammatory mediators, including TNF alpha, IL-1 beta, IL-6, and IFN-gamma. There are conflicting reports on the role of IL-33 in bone homeostasis, with some demonstrating a bone protective role for IL-33 whilst others show that IL-33 induces inflammatory arthritis with concurrent bone destruction. To better clarify the role IL-33 plays in bone biology in vivo, we studied IL-33 KO mice as well as mice in which the cytokine form of IL-33 was overexpressed. Mid femur cortical bone mineral density (BMD) and bone strength were similar in the IL-33 KO mice compared to WT animals during the first 8 months of life. However, in the absence of IL-33, we observed higher BMD in lumbar vertebrae and distal femur in female mice. In contrast, overexpression of IL-33 resulted in a marked and rapid reduction of bone volume, mineral density and strength. Moreover, this was associated with a robust increase in inflammatory cytokines (including IL-6 and IFN-gamma), suggesting the bone pathology could be a direct effect of IL-33 or an indirect effect due to the induction of other mediators. Furthermore, the detrimental bone effects were accompanied by increases in osteoclast number and the bone resorption marker of C-terminal telopeptide collagen-I (CTX-I). Together, these results demonstrate that absence of IL-33 has no negative consequences in normal bone homeostasis while high levels of circulating IL-33 contributes to pathological bone loss. (C) 2015 Elsevier Ltd. All rights reserved.
机译：白介素（IL）-33是IL-1家族的成员。 IL-33的作用是通过其受体ST2和IL-1RAcP介导的，其信号传导诱导了多种促炎性介质的产生，包括TNFα，IL-1β，IL-6和IFN-γ。关于IL-33在骨稳态中的作用有相互矛盾的报道，有的证明了IL-33对骨骼的保护作用，而另一些则表明IL-33诱发了炎症性关节炎，并发了骨破坏。为了更好地阐明IL-33在体内骨骼生物学中的作用，我们研究了IL-33 KO小鼠以及其中细胞因子形式的IL-33过表达的小鼠。在生命的头8个月中，与野生型动物相比，IL-33 KO小鼠的股骨中层皮质骨矿物质密度（BMD）和骨强度相似。但是，在没有IL-33的情况下，我们观察到雌性小鼠腰椎和股骨远端的BMD较高。相反，IL-33的过表达导致骨骼体积，矿物质密度和强度显着而迅速的降低。此外，这与炎性细胞因子（包括IL-6和IFN-γ）的强劲增加有关，表明骨骼病理可能是IL-33的直接作用或由于其他介质的诱导而产生的间接作用。此外，有害的骨效应伴随着破骨细胞数量的增加和C末端端肽胶原蛋白I（CTX-1）的骨吸收标记物的增加。总之，这些结果表明，IL-33的缺乏对正常的骨稳态没有负面影响，而循环中的IL-33的高水平则导致病理性骨丢失。 （C）2015 Elsevier Ltd.保留所有权利。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号