Fatty acid oxidation participates in resistance to nutrient-depleted environments in the insect stages of Trypanosoma cruzi (Pub Date: 2021-04-05)

https://doi.org/10.1371/journal.ppat.1009495

Fatty acid oxidation participates in resistance to nutrient-depleted environments in the insect stages of Trypanosoma cruzi

Abstract

Trypanosoma cruzi, the parasite causing Chagas disease, is a digenetic flagellated protist that infects mammals (including humans) and reduviid insect vectors. Therefore, T. cruzi must colonize different niches in order to complete its life cycle in both hosts. This fact determines the need of adaptations to face challenging environmental cues. The primary environmental challenge, particularly in the insect stages, is poor nutrient availability. In this regard, it is well known that T. cruzi has a flexible metabolism able to rapidly switch from carbohydrates (mainly glucose) to amino acids (mostly proline) consumption. Also established has been the capability of T. cruzi to use glucose and amino acids to support the differentiation process occurring in the insect, from replicative non-infective epimastigotes to non-replicative infective metacyclic trypomastigotes. However, little is known about the possibilities of using externally available and internally stored fatty acids as resources to survive in nutrient-poor environments, and to sustain metacyclogenesis. In this study, we revisit the metabolic fate of fatty acid breakdown in T. cruzi. Herein, we show that during parasite proliferation, the glucose concentration in the medium can regulate the fatty acid metabolism. At the stationary phase, the parasites fully oxidize fatty acids. [U-14C]-palmitate can be taken up from the medium, leading to CO2 production. Additionally, we show that electrons are fed directly to oxidative phosphorylation, and acetyl-CoA is supplied to the tricarboxylic acid (TCA) cycle, which can be used to feed anabolic pathways such as the de novo biosynthesis of fatty acids. Finally, we show as well that the inhibition of fatty acids mobilization into the mitochondrion diminishes the survival to severe starvation, and impairs metacyclogenesis. Author summary: Trypanosoma cruzi is a protist parasite with a life cycle involving two types of hosts, a vertebrate one (which includes humans, causing Chagas disease) and an invertebrate one (kissing bugs, which vectorize the infection among mammals). In both hosts, the parasite faces environmental challenges such as sudden changes in the metabolic composition of the medium in which they develop, sever

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Comparative analysis of ketone body metabolism in BALB/c mice infected with Trypanosoma evansi and Toxoplasma gondii. (Pub Date: 2021-12-20)

https://doi.org/10.1016/j.rvsc.2021.12.016

https://pubmed.ncbi.nlm.nih.gov/35026630

Abstract

KBs (ketone bodies), i.e., acetoacetate, acetone, and (R)-3-Hydroxybutanoate, constitute the intermediate products of the incomplete oxidative degradation of fatty acids. These KBs are used as a source of energy in the hosts' brain, skeletal muscles, and heart. Additionally, they regulate inflammation and oxidative stress of the host by acting as signaling mediators. Parasitic infection is known to result in abnormal physiological and biochemical metabolism, ketoacidosis, and other damage to the host. In this study, we investigated the effects of Trypanosoma evansi and Toxoplasma gondii on ketone body metabolism in mice, as well as the KB levels in the brain, liver, and peripheral blood. T. gondii was found to significantly increase the KB levels, resulting in ketonemia, T. evansi was found to stabilize KB levels in mice. Further investigations showed that T. evansi downregulated the expression of genes encoding enzymes involved in KBs synthesizing pathway and enhanced KBs synthesizing to eliminate ketonemia. Conversely, T. gondii significantly increased the expression of genes encoding enzymes involved in KBs synthesizing pathway and decreased KBs metabolism pathway ones and resulting in increased KBs levels in peripheral blood, culminating in ketonemia. These findings elucidate the differences in the KBs metabolism resulting from infection with T. evansi and T. gondii.

------------------------------------------ Info ------------------------------------------

Open Access: False

Authors: Zhaobo Zhang - Yifan Li - Ning Jiang - Xiaoyu Sang - Limei Han -

Additional links: None found

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How do you tell the difference between the Trypomastigote in blood smear of Trypanosoma cruzi and Trypanosoma brucei?

What are their unique Trypomastigote appearance characteristics? How can I differentiate them based on blood smear alone?

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A Triatominae ("Kissing Bug") drawn by my great-grandmother for my great-grandfather, who studied the Chagas disease. The disease is caused by the Trypanosoma cruzi parasite, carried by these bugs.
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Is anyone familiar with Trypanosoma cruzi? /r/ecology/comments/k8ixr…
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Maxicircle architecture and evolutionary insights into Trypanosoma cruzi complex: https://doi.org/10.1371/journal.pntd.0009719
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Maxicircle architecture and evolutionary insights into Trypanosoma cruzi complex: https://doi.org/10.1371/journal.pntd.0009719
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Single-cell transcriptomic analysis of bloodstream Trypanosoma brucei reconstructs cell cycle progression and developmental quorum sensing: https://www.nature.com/articles/s41467-021-25607-2
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AMERICAN SCIENTISTS CONFIRM GRAPHENE OXIDE IN VACCINES, PFIZER CONTAINS TRYPANOSOMA CRUZI PARASITE thepeoplesvoice.org/TPV3/…
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Quantification of RNA Polymerase I transcriptional attenuation at the active VSG expression site in Trypanosoma brucei biorxiv.org/content/10.11…
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Blood sample of a patient infected with Trypanosoma cruzi, Chagas disease
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Somebody’s happy to see me this morning! Trypanosoma brucei on a hemocytometer. v.redd.it/v12j1b66rfk61
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