Giardia duodenalis stabilizes HIF-1α and induces glycolytic alterations in intestinal epithelial cells

Abstract The gastrointestinal epithelium relies on activation of the hypoxia-inducible factor (HIF) to promote cell survival and maintain bioenergetic homeostasis during hypoxia. While many pathogens can activate HIF, the effects of enteric protozoa on HIF activation in gastrointestinal epithelial c...

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Main Authors: Emily DeMichele, Olivia Sosnowski, Darragh Flood, Cormac T. Taylor, Ian A. Lewis, Thibault Allain, Andre G. Buret
Format: Article
Language:English
Published: Nature Portfolio 2025-08-01
Series:Scientific Reports
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Online Access:https://doi.org/10.1038/s41598-025-13635-7
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author Emily DeMichele
Olivia Sosnowski
Darragh Flood
Cormac T. Taylor
Ian A. Lewis
Thibault Allain
Andre G. Buret
author_facet Emily DeMichele
Olivia Sosnowski
Darragh Flood
Cormac T. Taylor
Ian A. Lewis
Thibault Allain
Andre G. Buret
author_sort Emily DeMichele
collection DOAJ
description Abstract The gastrointestinal epithelium relies on activation of the hypoxia-inducible factor (HIF) to promote cell survival and maintain bioenergetic homeostasis during hypoxia. While many pathogens can activate HIF, the effects of enteric protozoa on HIF activation in gastrointestinal epithelial cells remain unclear. Giardia duodenalis, a prevalent protozoan enteropathogen, causes intestinal barrier dysfunction characterized by epithelial malabsorption, mucus depletion, altered mucin glycosylation, and microbiota dysbiosis. Findings from the present study reveal an epithelial hypoxic signature upon Giardia infection. Human intestinal epithelial cells were exposed to vehicle or Giardia duodenalis isolate GS/M under normoxic (21% O2) or hypoxic (1% O2) conditions. In normoxia, infected cells displayed a time-dependent increase in HIF-1α protein expression, the oxygen-dependent subunit of HIF-1. In normoxia, Giardia infection upregulated HIF-1 target genes involved in cellular stress (i.e., VEGFA, ANKRD37, GADD45A) and glycolysis (i.e., HK2, LDHA). This was accompanied by changes in the abundance of glycolytic intermediates (i.e., glucose-6-phosphate, pyruvate, lactate). Although infection in hypoxia failed to augment the hypoxia-induced HIF-1α stabilization, HIF-1 target genes were still upregulated, albeit to a lesser degree. These findings indicate that Giardia induces a transient epithelial hypoxic response in normoxic conditions, revealing a hitherto unrecognized epithelial rescue response to this intestinal parasite.
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spelling doaj-art-f70eb49e07ba45d085ff67f46b48acf92025-08-20T03:42:38ZengNature PortfolioScientific Reports2045-23222025-08-0115111210.1038/s41598-025-13635-7Giardia duodenalis stabilizes HIF-1α and induces glycolytic alterations in intestinal epithelial cellsEmily DeMichele0Olivia Sosnowski1Darragh Flood2Cormac T. Taylor3Ian A. Lewis4Thibault Allain5Andre G. Buret6Department of Biological Sciences, University of CalgaryDepartment of Biological Sciences, University of CalgaryThe Conway Institute, School of Medicine and Systems Biology Ireland, University College DublinThe Conway Institute, School of Medicine and Systems Biology Ireland, University College DublinDepartment of Biological Sciences, University of CalgaryDepartment of Biological Sciences, University of CalgaryDepartment of Biological Sciences, University of CalgaryAbstract The gastrointestinal epithelium relies on activation of the hypoxia-inducible factor (HIF) to promote cell survival and maintain bioenergetic homeostasis during hypoxia. While many pathogens can activate HIF, the effects of enteric protozoa on HIF activation in gastrointestinal epithelial cells remain unclear. Giardia duodenalis, a prevalent protozoan enteropathogen, causes intestinal barrier dysfunction characterized by epithelial malabsorption, mucus depletion, altered mucin glycosylation, and microbiota dysbiosis. Findings from the present study reveal an epithelial hypoxic signature upon Giardia infection. Human intestinal epithelial cells were exposed to vehicle or Giardia duodenalis isolate GS/M under normoxic (21% O2) or hypoxic (1% O2) conditions. In normoxia, infected cells displayed a time-dependent increase in HIF-1α protein expression, the oxygen-dependent subunit of HIF-1. In normoxia, Giardia infection upregulated HIF-1 target genes involved in cellular stress (i.e., VEGFA, ANKRD37, GADD45A) and glycolysis (i.e., HK2, LDHA). This was accompanied by changes in the abundance of glycolytic intermediates (i.e., glucose-6-phosphate, pyruvate, lactate). Although infection in hypoxia failed to augment the hypoxia-induced HIF-1α stabilization, HIF-1 target genes were still upregulated, albeit to a lesser degree. These findings indicate that Giardia induces a transient epithelial hypoxic response in normoxic conditions, revealing a hitherto unrecognized epithelial rescue response to this intestinal parasite.https://doi.org/10.1038/s41598-025-13635-7GiardiaGiardiasisIntestinal epithelial cellsHypoxiaHIF-1αGlycolysis
spellingShingle Emily DeMichele
Olivia Sosnowski
Darragh Flood
Cormac T. Taylor
Ian A. Lewis
Thibault Allain
Andre G. Buret
Giardia duodenalis stabilizes HIF-1α and induces glycolytic alterations in intestinal epithelial cells
Scientific Reports
Giardia
Giardiasis
Intestinal epithelial cells
Hypoxia
HIF-1α
Glycolysis
title Giardia duodenalis stabilizes HIF-1α and induces glycolytic alterations in intestinal epithelial cells
title_full Giardia duodenalis stabilizes HIF-1α and induces glycolytic alterations in intestinal epithelial cells
title_fullStr Giardia duodenalis stabilizes HIF-1α and induces glycolytic alterations in intestinal epithelial cells
title_full_unstemmed Giardia duodenalis stabilizes HIF-1α and induces glycolytic alterations in intestinal epithelial cells
title_short Giardia duodenalis stabilizes HIF-1α and induces glycolytic alterations in intestinal epithelial cells
title_sort giardia duodenalis stabilizes hif 1α and induces glycolytic alterations in intestinal epithelial cells
topic Giardia
Giardiasis
Intestinal epithelial cells
Hypoxia
HIF-1α
Glycolysis
url https://doi.org/10.1038/s41598-025-13635-7
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