Open AccessGLUT1‐mediated glucose uptake plays a crucial role during Plasmodium hepatic infection
Author(s) -
Meireles Patrícia,
SalesDias Joana,
Andrade Carolina M.,
MelloVieira João,
MancioSilva Liliana,
Simas J. Pedro,
Staines Henry M.,
Prudêncio Miguel
Publication year - 2017
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/cmi.12646
Subject(s) - glut1 , biology , plasmodium berghei , glucose transporter , in vivo , glucose uptake , in vitro , transporter , intracellular , plasmodium (life cycle) , microbiology and biotechnology , parasite hosting , cell , intracellular parasite , biochemistry , malaria , immunology , gene , endocrinology , genetics , insulin , world wide web , computer science
Summary Intracellular pathogens have evolved mechanisms to ensure their survival and development inside their host cells. Here, we show that glucose is a pivotal modulator of hepatic infection by the rodent malaria parasite Plasmodium berghei and that glucose uptake via the GLUT1 transporter is specifically enhanced in P . berghei ‐infected cells. We further show that ATP levels of cells containing developing parasites are decreased, which is known to enhance membrane GLUT1 activity. In addition, GLUT1 molecules are translocated to the membrane of the hepatic cell, increasing glucose uptake at later stages of infection. Chemical inhibition of GLUT1 activity leads to a decrease in glucose uptake and the consequent impairment of hepatic infection, both in vitro and in vivo . Our results reveal that changes in GLUT1 conformation and cellular localization seem to be part of an adaptive host response to maintain adequate cellular nutrition and energy levels, ensuring host cell survival and supporting P . berghei hepatic development.