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Pathogens
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Trypanosoma cruzi Infection: Cellular and Molecular Basis
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Trypanosoma cruzi Infection: Cellular and Molecular Basis

A special issue of Pathogens (ISSN 2076-0817). This special issue belongs to the section "Parasitic Pathogens".

Deadline for manuscript submissions: 30 April 2025 | Viewed by 2018

Special Issue Editors

Dr. Guozhong Huang

E-Mail Website
Guest Editor
Center for Tropical and Emerging Global Diseases, University of Georgia, Athens, GA, USA
Interests: trypanosomes; calcium signaling; chemotherapy
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Roberto Docampo

E-Mail Website
Guest Editor
1. Center for Tropical and Emerging Global Diseases, University of Georgia, Athens, GA 30602, USA
2. Department of Cellular Biology, University of Georgia, Athens, GA 30602, USA
Interests: metabolic pathways of trypanosomatids and malaria parasites

Special Issue Information

Dear Colleagues,

Trypanosoma cruzi, the causative agent of Chagas disease (also called American trypanosomiasis), is a parasitic protist that affects millions of people worldwide. No vaccines are available to prevent this disease, and current drug treatments have serious side effects and are not completely effective. The survival of T. cruzi in the mammalian hosts depends on the parasite's ability to infect host cells, reproduce, and live in the blood of the host long enough to warrant is transmission through a bloodsucking insect vector. However, as few genetic tools are available to work with T. cruzi, the cellular, biochemical, and molecular mechanisms for the pathogenesis of this parasite’s infection have not been completely known. Elucidating the cellular and molecular basis of T. cruzi infections will not only provide important information for better understanding the parasite–host interactions but also discover new potential drug targets for the prevention of this parasite in humans. With the recent application of the CRISPR/cas9 technique for gene knockout, gene downregulation, and endogenous gene tagging in T. cruzi, our research is making tremendous advances in defining its pathogenetic machinery. The scope of this Special Issue includes the identification and characterization of cell structures, organelles, genes, enzymes, transporters, or metabolic pathways required for the process of T. cruzi infection. We will accept reviews or original contributions.

Dr. Guozhong Huang
Prof. Dr. Roberto Docampo
Guest Editors

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Pathogens is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Trypanosoma cruzi
  • Chagas disease
  • trypanosomiasis
  • pathogenesis
  • drug target
  • CRISPR/cas9
  • gene knockout
  • downregulation
  • gene tagging

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Published Papers (2 papers)

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Research

17 pages, 5643 KiB  
Article
Differential Regulation of L-Arginine Metabolism through NOS2 and Arginases during Infection with Trypanosoma cruzi
by Arturo A. Wilkins-Rodríguez, Paz María Salazar-Schettino, Rebeca G. Manning-Cela and Laila Gutiérrez-Kobeh
Pathogens 2024, 13(10), 878; https://doi.org/10.3390/pathogens13100878 - 8 Oct 2024
Viewed by 884
Abstract
L-arginine metabolism through arginases and inducible nitric oxide synthase (NOS2) constitutes a fundamental axis for the resolution or progression of Chagas disease. Infection with Trypanosoma cruzi can cause a wide spectrum of disease, ranging from acute forms contained by the host immune response [...] Read more.
L-arginine metabolism through arginases and inducible nitric oxide synthase (NOS2) constitutes a fundamental axis for the resolution or progression of Chagas disease. Infection with Trypanosoma cruzi can cause a wide spectrum of disease, ranging from acute forms contained by the host immune response to chronic ones, such as the chronic chagasic cardiomyopathy. Here, we analyzed, in an in vitro model, the ability of two T. cruzi isolates, with different degrees of virulence, to regulate the metabolism of L-arginine through arginase 1 (Arg-1) and NOS2 in macrophages and through arginase 2 (Arg-2) and NOS2 in cardiomyocytes. Stimulation of bone marrow-derived macrophages (BMMΦ), obtained from CD1 mice, with TNF-α + IFN-γ induced their polarization into classically activated macrophages (CAMΦ), which expressed functional NOS2, while stimulation with IL-4 induced their polarization into alternatively activated macrophages (AAMΦ), which expressed functional Arg-1. Interestingly, stimulation of cardiomyocytes, obtained from hearts of CD1 neonatal mice, with TNF-α + IFN-γ or IL-4 also resulted in functional NOS2 and arginase expression, as observed in CAMΦ and AAMΦ, but Arg-2 was the arginase isoform expressed instead of Arg-1. We observed that infection of BMMΦ with the more virulent T. cruzi isolate (QRO) importantly diminished NOS2 expression and nitric oxide (NO) production in CAMΦ, allowing parasite survival, while infection with the less virulent isolate (CI2) did not diminish NOS2 activity and NO production in CAMΦ to a great extent, which resulted in parasite killing. Regarding Arg-1, infection of BMMΦ with the QRO isolate significantly induced Arg-1 expression and activity in AAMΦ, which resulted in a higher parasite load than the one in the unstimulated BMMΦ. Even though infection with CI2 isolate did not increase Arg-1 expression and activity in AAMΦ, the parasite load was higher than the one in the unstimulated BMMΦ but at a lesser magnitude than that observed during infection with the QRO isolate. On the other hand, infection of cardiomyocytes with either QRO or CI2 isolates and further stimulation with TNF-α + IFN-γ inhibited NOS2 expression and NO production, leading to amelioration of infection. Surprisingly, infection of cardiomyocytes with either QRO or CI2 isolates and further stimulation with IL-4 strongly inhibited Arg-2 expression and function, which resulted in parasite loads similar to those observed in unstimulated cardiomyocytes. Our results suggest that T. cruzi isolates that exhibit variable virulence or pathogenicity degrees differentially regulate L-arginine metabolism through Arg-1/2 and NOS2 in macrophages and cardiomyocytes. Full article
(This article belongs to the Special Issue Trypanosoma cruzi Infection: Cellular and Molecular Basis)
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11 pages, 4312 KiB  
Article
Inorganic Polyphosphate Is in the Surface of Trypanosoma cruzi but Is Not Significantly Secreted
by Logan P. Crowe, Anna Gioseffi, Mayara S. Bertolini and Roberto Docampo
Pathogens 2024, 13(9), 776; https://doi.org/10.3390/pathogens13090776 - 9 Sep 2024
Viewed by 777
Abstract
Trypanosoma cruzi is the etiologic agent of Chagas disease, an infection that can lead to the development of cardiac fibrosis, which is characterized by the deposition of extracellular matrix (ECM) components in the interstitial region of the myocardium. The parasite itself can induce [...] Read more.
Trypanosoma cruzi is the etiologic agent of Chagas disease, an infection that can lead to the development of cardiac fibrosis, which is characterized by the deposition of extracellular matrix (ECM) components in the interstitial region of the myocardium. The parasite itself can induce myofibroblast differentiation of cardiac fibroblast in vitro, leading to increased expression of ECM. Inorganic polyphosphate (polyP) is a linear polymer of orthophosphate that can also induce myofibroblast differentiation and deposition of ECM components and is highly abundant in T. cruzi. PolyP can modify proteins post-translationally by non-enzymatic polyphosphorylation of lysine residues of poly-acidic, serine-(S) and lysine (K)-rich (PASK) motifs. In this work, we used a bioinformatics screen and identified the presence of PASK domains in several surface proteins of T. cruzi. We also detected polyP in the external surface of its different life cycle stages and confirmed the stimulation of host cell fibrosis by trypomastigote infection. However, we were not able to detect significant secretion of the polymer or activation of transforming growth factor beta (TGF-β), an important factor for the generation of fibrosis by inorganic polyP- or trypomastigote-conditioned medium. Full article
(This article belongs to the Special Issue Trypanosoma cruzi Infection: Cellular and Molecular Basis)
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