Infection with Mycobacterium avium differentially regulates the expression of iron transport protein mRNA in murine peritoneal macrophages.
Infection with Mycobacterium avium differentially regulates the expression of iron transport protein mRNA in murine peritoneal macrophages.
复制标题
鸟分枝杆菌感染差异调节小鼠腹膜巨噬细胞中铁转运蛋白 mRNA 的表达。
DOI：
10.1128/iai.69.11.6618-6624.2001
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发表时间：
2001
影响因子：
3.1
通讯作者：
Zwilling,BS
中科院分区：
文献类型：
--
作者：
Zhong,W;Lafuse,WP;Zwilling,BS
铁是微生物生长和防御宿主的重要元素，它是通过Fenton/Haber-Weiss反应产生自由基的催化剂。铁转运体天然耐药相关巨噬细胞蛋白1(Nramp1)对包括禽分枝杆菌在内的多种细胞内病原体的生长具有抵抗力。最近，还描述了与铁转运有关的其他几种蛋白质，包括高度同源的铁转运蛋白Nramp2和转铁蛋白受体相关蛋白HFE(遗传性血色沉着病蛋白)。这些蛋白与宿主防御和细胞内病原体生长的关系尚不清楚。在这里，我们报告感染M。铁转运相关蛋白在小鼠腹膜巨噬细胞中的差异表达。感染后Nramp1和Nramp2的mRNA水平均升高，而转铁蛋白受体的mRNA表达下降。HFe基因的表达水平无明显变化。这些蛋白在感染或细胞因子刺激后表达的差异表明，它们可能在宿主防御中发挥重要作用，在用于宿主防御的铁可利用性和同时限制用于微生物生长的铁之间保持微妙的平衡。
Iron is an important element for the growth of microorganisms as well as in the defense of the host by serving as a catalyst for the generation of free radicals via the Fenton/Haber-Weiss reactions. The iron transporter natural resistance-associated macrophage protein 1 (Nramp1) confers resistance to the growth of a variety of intracellular pathogens includingMycobacterium avium. Recently several other proteins that are involved in iron transport, including the highly homologous iron transporter Nramp2 and the transferrin receptor-associated protein HFE (hereditary hemochromatosis protein), have been described. The relationship of these proteins to host defense and to the growth of intracellular pathogens is not known. Here, we report that infection withM. aviumdifferentially regulates mRNA expression of the proteins associated with iron transport in murine peritoneal macrophages. Both Nramp1 and Nramp2 mRNA levels increase following infection, while the expression of transferrin receptor mRNA decreases. The level of expression of HFE mRNA remains unchanged. The difference in the expression of the mRNA of these proteins following infection or cytokine stimulation suggests that they may play an important role in host defense by maintaining a delicate balance between iron availability for host defense and at the same time limiting iron availability for microbial growth.