Litcius/Paper detail

The Absence of HIF-1α Increases Susceptibility to Leishmania donovani Infection via Activation of BNIP3/mTOR/SREBP-1c Axis

Inês Mesquita, Carolina Ferreira, Diana Moreira, George Eduardo Gabriel Kluck, Ana Margarida Barbosa, Egídio Torrado, Ricardo Jorge Dinis‐Oliveira, Luís G. Gonçalves, Charles-Joly Beauparlant, Arnaud Droit, Luciana Berod, Tim Sparwasser, Neelam Bodhale, Bhaskar Saha, Fernando Rodrigues, Cristina Cunha, Agostinho Carvalho, António G. Castro, Jérôme Estaquier, Ricardo Silvestre

2020Cell Reports48 citationsDOIOpen Access PDF

Abstract

macrophages. L. donovani-infected HIF-1α-deficient mice develop hypertriglyceridemia and lipid accumulation in splenic and hepatic myeloid cells. Most importantly, our data demonstrate that manipulating FASN or SREBP-1c using pharmacological inhibitors significantly reduced parasite burden. As such, genetic deficiency of HIF-1α is associated with increased lipid accumulation, which results in impaired host-protective anti-leishmanial functions of myeloid cells.

Topics & Concepts

Leishmania donovaniBiologyLipogenesisLipid metabolismCell biologyInnate immune systemMyeloidSterol regulatory element-binding proteinPI3K/AKT/mTOR pathwaymTORC2Immune systemCancer researchImmunologyTranscription factormTORC1Signal transductionBiochemistryGeneLeishmaniasisVisceral leishmaniasisResearch on Leishmaniasis StudiesPancreatitis Pathology and TreatmentLysosomal Storage Disorders Research