Abstract
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.
Highlights
Transmissible gastroenteritis (TGE) is a highly contagious infectious disease of pigs that is characterized by vomiting, diarrhea, and dehydration
The effects of coronaviruses on glucose uptake have not been reported. we found that TGE virus (TGEV) infection increased glucose uptake of IPEC-J2 cells and the protein expression of SGLT1, glucose transporter 2 (GLUT2) after 48 hpi (Fig 1), while TGEV infection in IPEC-J2 cells reached a peak at 48 hpi [31], we just provided foresight to explore the interaction between TGEV infection and glucose uptake, which is still worth exploring
Most of the glucose absorbed in the intestine is transformed to glutamine [32], which was reported to promote the replication of many viruses, such as porcine circovirus (PCV) and human cytomegalovirus (HCMV), in vitro [33, 34]
Summary
Transmissible gastroenteritis (TGE) is a highly contagious infectious disease of pigs that is characterized by vomiting, diarrhea, and dehydration. The mortality rate of this disease in seronegative suckling piglets can reach up to 100% [1]. Glucose is among the nutrients absorbed in the intestinal epithelium, and glucose uptake in epithelial cells depends on two types of glucose transporters, the apically expressed Na+-dependent glucose transporter 1 (SGLT1) and basolaterally expressed facilitative glucose transporter 2 (GLUT2). SGLT1 mediates the Na+/glucose cotransport function of the kidney and intestine as a secondary active transporter, while GLUT2 serves as a facilitated diffusion system for transport through lipid bilayers [4,5,6]. A recently study suggested that EGFR may act as another receptor for TGEV, in addition to porcine aminopeptidase (pAPN) [9]. EGFR-dependent regulation of glucose uptake has been observed in tumor cells, and EGFR has been shown to prevent autophagic cell death by maintaining intracellular glucose levels through interaction with and stabilization of SGLT1 [10]
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