Selenium attenuates pro-inflammatory gene expression in macrophages
Selenium attenuates pro-inflammatory gene expression in macrophages
复制标题
DOI：
10.1002/mnfr.200700346
复制
发表时间：
2008-11-01
影响因子：
5.2
通讯作者：
Prabhu, K. Sandeep
中科院分区：
文献类型：
--
作者：
Vunta, Hema;Belda, Benjamin J.;Prabhu, K. Sandeep
硒(Se)是免疫系统最佳功能所必需的重要元素。特别是在免疫调节中起关键作用的巨噬细胞中，硒以硒蛋白的形式发挥主要抗氧化剂的作用，以减轻活性氧的细胞毒性效应。本文介绍了硒的抗炎作用及其对细菌内毒素诱导的巨噬细胞信号转导通路的影响。我们的研究表明，向巨噬细胞补充硒(缺硒)可显著降低内毒素诱导的两个重要的促炎基因环氧合酶-2(COX-2)和肿瘤坏死因子-α(TNF-α)的表达，这是通过抑制MAP激酶途径实现的。此外，小鼠的缺硒加剧了内毒素介导的巨噬细胞对肺的渗透，这表明硒状态是调节炎症的关键宿主因素。综上所述，我们的结果表明，硒作为一种抗炎剂，通过严格调控免疫细胞中促炎症基因的表达，发挥了重要的作用。
Selenium (Se) is an important element required for the optimal functioning of the immune system. Particularly in macrophages, which play a pivotal role in immune regulation, Se acts as a major antioxidant in the form of selenoproteins to mitigate the cytotoxic effects of reactive oxygen species. Here we describe the role of Se as an anti-inflammatory agent and its effect on the macrophage signal transduction pathways elicited by bacterial endotoxin, LPS. Our studies demonstrate that supplementation of Se to macrophages (Se-deficient) leads to a significant decrease in the LPS-induced expression of two important pro-inflammatory genes, cyclooxygenase-2 (COX-2) and tumor necrosis factor-alpha (TNF-alpha) via the inhibition of MAP kinase pathways. Furthermore, Se-deficiency in mice exacerbated the LPS-mediated infiltration of macrophages into the lungs suggesting that Se status is a crucial host factor that regulates inflammation. In summary, our results indicate that Se plays an important role as an anti-inflammatory agent by tightly regulating the expression of pro-inflammatory genes in immune cells.