Publications by authors named "Marta Reverte"

3 Publications

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The antioxidant response favors Leishmania parasites survival, limits inflammation and reprograms the host cell metabolism.

PLoS Pathog 2021 Mar 25;17(3):e1009422. Epub 2021 Mar 25.

Department of Biochemistry, University of Lausanne, Epalinges, Switzerland.

The oxidative burst generated by the host immune system can restrict intracellular parasite entry and growth. While this burst leads to the induction of antioxidative enzymes, the molecular mechanisms and the consequences of this counter-response on the life of intracellular human parasites are largely unknown. The transcription factor NF-E2-related factor (NRF2) could be a key mediator of antioxidant signaling during infection due to the entry of parasites. Here, we showed that NRF2 was strongly upregulated in infection with the human Leishmania protozoan parasites, its activation was dependent on a NADPH oxidase 2 (NOX2) and SRC family of protein tyrosine kinases (SFKs) signaling pathway and it reprogrammed host cell metabolism. In inflammatory leishmaniasis caused by a viral endosymbiont inducing TNF-α in chronic leishmaniasis, NRF2 activation promoted parasite persistence but limited TNF-α production and tissue destruction. These data provided evidence of the dual role of NRF2 in protecting both the invading pathogen from reactive oxygen species and the host from an excess of the TNF-α destructive pro-inflammatory cytokine.
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http://dx.doi.org/10.1371/journal.ppat.1009422DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7993605PMC
March 2021

Parasite Quantification by Bioluminescence in Murine Models.

Bio Protoc 2019 Nov 20;9(22):e3431. Epub 2019 Nov 20.

Department of Biochemistry, University of Lausanne, Epalinges, Switzerland.

Leishmaniasis remains a major public health problem worldwide with a prevalence of 12 million, an incidence of 1 million persons, and 350 million people being at risk. Murine models have been largely used for studying the host-pathogen relationship and developing effective chemotherapies against parasites. Thus, preclinical imaging is crucial for monitoring the disease outcome. The aim of this protocol is to quantify parasite burden using bioluminescence imaging. Here, we describe a high-throughput imaging workflow, together with data acquisition and analysis ideal to assess parasite load in mouse models.
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http://dx.doi.org/10.21769/BioProtoc.3431DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7853991PMC
November 2019

Mammalian Innate Immune Response to a Leishmania-Resident RNA Virus Increases Macrophage Survival to Promote Parasite Persistence.

Cell Host Microbe 2016 Sep 1;20(3):318-328. Epub 2016 Sep 1.

Department of Biochemistry, University of Lausanne, 1066 Epalinges, Switzerland. Electronic address:

Some strains of the protozoan parasite Leishmania guyanensis (L.g) harbor a viral endosymbiont called Leishmania RNA virus 1 (LRV1). LRV1 recognition by TLR-3 increases parasite burden and lesion swelling in vivo. However, the mechanisms by which anti-viral innate immune responses affect parasitic infection are largely unknown. Upon investigating the mammalian host's response to LRV1, we found that miR-155 was singularly and strongly upregulated in macrophages infected with LRV1+ L.g when compared to LRV1- L.g. LRV1-driven miR-155 expression was dependent on TLR-3/TRIF signaling. Furthermore, LRV1-induced TLR-3 activation promoted parasite persistence by enhancing macrophage survival through Akt activation in a manner partially dependent on miR-155. Pharmacological inhibition of Akt resulted in a decrease in LRV1-mediated macrophage survival and consequently decreased parasite persistence. Consistent with these data, miR-155-deficient mice showed a drastic decrease in LRV1-induced disease severity, and lesional macrophages from these mice displayed reduced levels of Akt phosphorylation.
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http://dx.doi.org/10.1016/j.chom.2016.08.001DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5493041PMC
September 2016