Dai Lei, Hu Wei Wei, Xia Lu, Xia Mi, Yang Qian
Veterinary College, Nanjing Agricultural University, Weigang 1, Nanjing, Jiangsu, PR China.
PLoS One. 2016 Nov 16;11(11):e0165585. doi: 10.1371/journal.pone.0165585. eCollection 2016.
Transmissible gastroenteritis virus (TGEV) is a coronavirus that causes villus atrophy, followed by crypt hyperplasia, reduces the activities of intestinal digestive enzymes, and disrupts the absorption of intestinal nutrients. In vivo, TGEV primarily targets and infects intestinal epithelial cells, which play an important role in glucose absorption via the apical and basolateral transporters Na+-dependent glucose transporter 1 (SGLT1) and facilitative glucose transporter 2 (GLUT2), respectively. In this study, we therefore sought to evaluate the effects of TGEV infection on glucose uptake and SGLT1 and GLUT2 expression. Our data demonstrate that infection with TGEV resulted in increased glucose uptake and augmented expression of EGFR, SGLT1 and GLUT2. Moreover, inhibition studies showed that EGFR modulated glucose uptake in control and TGEV infected cells. Finally, high glucose absorption was subsequently found to promote TGEV replication.
传染性胃肠炎病毒(TGEV)是一种冠状病毒,可导致绒毛萎缩,继而隐窝增生,降低肠道消化酶活性,并扰乱肠道营养物质的吸收。在体内,TGEV主要靶向并感染肠道上皮细胞,这些细胞分别通过顶端和基底外侧转运体——钠依赖性葡萄糖转运体1(SGLT1)和易化葡萄糖转运体2(GLUT2)在葡萄糖吸收中发挥重要作用。因此,在本研究中,我们试图评估TGEV感染对葡萄糖摄取以及SGLT1和GLUT2表达的影响。我们的数据表明,TGEV感染导致葡萄糖摄取增加以及表皮生长因子受体(EGFR)、SGLT1和GLUT2的表达增强。此外,抑制研究表明,EGFR调节对照细胞和TGEV感染细胞中的葡萄糖摄取。最后,随后发现高葡萄糖吸收促进TGEV复制。