Johnson Deborah, Bayele Henry, Johnston Kelly, Tennant Jason, Srai Surjit Kaila, Sharp Paul
School of Biomedical and Molecular Sciences, University of Surrey, Guildford GU2 7XH, UK.
FEBS Lett. 2004 Aug 27;573(1-3):195-201. doi: 10.1016/j.febslet.2004.07.081.
TNFalpha has dramatic effects on iron metabolism contributing to the generation of hypoferraemia in the anaemia of chronic disease. Interestingly, TNFalpha is also synthesised and released within the intestinal mucosa, suggesting that this pro-inflammatory cytokine may play a role in regulating dietary iron absorption. To investigate this possibility, we stimulated intestinal Caco-2 cells with TNFalpha (10 ng/ml). In TNFalpha-treated cells, apical iron uptake was significantly decreased and this was accompanied by a reduction in divalent metal transporter protein and mRNA expression. Our data suggest that TNFalpha could regulate dietary iron absorption and that the apical transport machinery is the target for these actions.
肿瘤坏死因子α(TNFα)对铁代谢具有显著影响,在慢性病贫血中导致低铁血症的产生。有趣的是,TNFα也在肠黏膜内合成并释放,这表明这种促炎细胞因子可能在调节膳食铁吸收中发挥作用。为了探究这种可能性,我们用TNFα(10纳克/毫升)刺激肠Caco-2细胞。在经TNFα处理的细胞中,顶端铁摄取显著降低,同时二价金属转运蛋白和mRNA表达也减少。我们的数据表明,TNFα可以调节膳食铁吸收,并且顶端转运机制是这些作用的靶点。