Flores Sebastian E, Aitchison Alan, Day Andrew S, Keenan Jacqueline I
Department of Surgery, University of Otago, Christchurch, New Zealand.
Department of Paediatrics, University of Otago, Christchurch, New Zealand.
PLoS One. 2017 Sep 5;12(9):e0184026. doi: 10.1371/journal.pone.0184026. eCollection 2017.
The iron deficiency anaemia that often accompanies infection with Helicobacter pylori may reflect increased uptake of iron into gastric epithelial cells. Here we show an infection-associated increase in total intracellular iron levels was associated with the redistribution of the transferrin receptor from the cell cytosol to the cell surface, and with increased levels of ferritin, an intracellular iron storage protein that corresponded with a significant increase in lysosomal stores of labile iron. In contrast, the pool of cytosolic labile iron was significantly decreased in infected cells. These changes in intracellular iron distribution were associated with the uptake and trafficking of H. pylori through the cells, and enhanced in strains capable of expressing the cagA virulence gene. We speculate that degradation of lysosomal ferritin may facilitate H. pylori pathogenesis, in addition to contributing to bacterial persistence in the human stomach.
经常伴随幽门螺杆菌感染出现的缺铁性贫血可能反映出铁向胃上皮细胞的摄取增加。在这里我们表明，感染相关的细胞内总铁水平升高与转铁蛋白受体从细胞溶质向细胞表面的重新分布有关，也与铁蛋白水平升高有关，铁蛋白是一种细胞内铁储存蛋白，其水平升高与不稳定铁的溶酶体储存显著增加相对应。相比之下，受感染细胞中细胞溶质不稳定铁池显著减少。细胞内铁分布的这些变化与幽门螺杆菌通过细胞的摄取和运输有关，并且在能够表达cagA毒力基因的菌株中增强。我们推测，溶酶体铁蛋白的降解可能有助于幽门螺杆菌的致病机制，此外还有助于细菌在人胃中的持续存在。
