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Pathogens
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Host-Pathogen Interaction Involved in Trypanosoma cruzi Infection
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Host-Pathogen Interaction Involved in Trypanosoma cruzi Infection

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

Deadline for manuscript submissions: closed (31 July 2021) | Viewed by 21647

Special Issue Editors

Dr. Ulrike Kemmerling

E-Mail Website
Guest Editor
Instituto de Ciencias Biomédicas, Facultad de Medicina, Universidad de Chile, Santiago de Chile 8380453, Chile
Interests: Trypanosoma cruzi; congenital Chagas disease; host–pathogen interaction
Special Issues, Collections and Topics in MDPI journals
Dr. Christian Castillo

E-Mail Website
Guest Editor
1. Instituto de Ciencias Biomédicas, Facultad de Medicina, Universidad de Chile, Santiago de Chile 8380453, Chile
2. Facultad de Medicina Veterinaria y Agronomía, Universidad de Las Américas, Santiago 7500975, Chile
Interests: Trypanosoma cruzi; congenital Chagas disease; chronic chagasic cardiopathy; host–pathogen interaction
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Chagas disease, or American trypanosomiasis, caused by the protozoan parasite Trypanosoma cruzi, is a silent, underdiagnosed and life-threatening disease. It constitutes a significant public health issue not only in Latin America, but also worldwide.

The probability of acquiring the disease depends on multiple factors: the parasite, the vectors, the mammalian hosts (including the human being), and socioeconomic aspects. Particularly, the host–pathogen interaction is a key factor determining the probability of infection and establishment of the disease. Thus, studying these different aspects is essential to understanding the pathogenesis of the disease and to improving the diagnostic and therapeutic tools for Trypanosoma cruzi infection. 

Therefore, for this Special Issue of Pathogens, we invite you to submit your contributions in the form of original research articles, review papers, and short communications about host-Trypanosoma cruzi interactions.

We look forward to your contributions and thank you very much for your collaboration.

Dr. Ulrike Kemmerling
Dr. Christian Castillo
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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 2700 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;
  • Host-parasite interaction;
  • Chagas disease treatment;
  • American trypanosomiasis

Published Papers (7 papers)

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Editorial

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2 pages, 184 KiB  
Editorial
Host–Pathogen Interaction Involved in Trypanosoma cruzi Infection
by Christian Castillo and Ulrike Kemmerling
Pathogens 2022, 11(5), 540; https://doi.org/10.3390/pathogens11050540 - 04 May 2022
Viewed by 1278
Abstract
Chagas disease, or American trypanosomiasis, caused by the protozoan parasite Trypanosoma cruzi (T. cruzi) [...] Full article
(This article belongs to the Special Issue Host-Pathogen Interaction Involved in Trypanosoma cruzi Infection)

Research

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14 pages, 2725 KiB  
Article
Ex Vivo Infection of Human Placental Explants by Trypanosoma cruzi Reveals a microRNA Profile Similar to That Seen in Trophoblast Differentiation
by Lisvaneth Medina, Jesús Alejandro Guerrero-Muñoz, Ana Isabel Liempi, Christian Castillo, Yessica Ortega, Alfredo Sepúlveda, Fernando Salomó, Juan Diego Maya and Ulrike Kemmerling
Pathogens 2022, 11(3), 361; https://doi.org/10.3390/pathogens11030361 - 16 Mar 2022
Cited by 5 | Viewed by 2093
Abstract
Congenital Chagas disease, caused by the protozoan parasite Trypanosoma cruzi, is responsible for 22.5% of new cases each year. However, placental transmission occurs in only 5% of infected mothers and it has been proposed that the epithelial turnover of the trophoblast can [...] Read more.
Congenital Chagas disease, caused by the protozoan parasite Trypanosoma cruzi, is responsible for 22.5% of new cases each year. However, placental transmission occurs in only 5% of infected mothers and it has been proposed that the epithelial turnover of the trophoblast can be considered a local placental defense against the parasite. Thus, Trypanosoma cruzi induces cellular proliferation, differentiation, and apoptotic cell death in the trophoblast, which are regulated, among other mechanisms, by small non-coding RNAs such as microRNAs. On the other hand, ex vivo infection of human placental explants induces a specific microRNA profile that includes microRNAs related to trophoblast differentiation such as miR-512-3p miR-515-5p, codified at the chromosome 19 microRNA cluster. Here we determined the expression validated target genes of miR-512-3p and miR-515-5p, specifically human glial cells missing 1 transcription factor and cellular FLICE-like inhibitory protein, as well as the expression of the main trophoblast differentiation marker human chorionic gonadotrophin during ex vivo infection of human placental explants, and examined how the inhibition or overexpression of both microRNAs affects parasite infection. We conclude that Trypanosoma cruzi-induced trophoblast epithelial turnover, particularly trophoblast differentiation, is at least partially mediated by placenta-specific miR-512-3p and miR-515-5p and that both miRNAs mediate placental susceptibility to ex vivo infection of human placental explants. Knowledge about the role of parasite-modulated microRNAs in the placenta might enable their use as biomarkers, as prognostic and therapeutic tools for congenital Chagas disease in the future. Full article
(This article belongs to the Special Issue Host-Pathogen Interaction Involved in Trypanosoma cruzi Infection)
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14 pages, 314 KiB  
Article
Chromatic and Morphological Differentiation of Triatoma dimidiata (Hemiptera: Reduviidae) with Land Use Diversity in El Salvador
by Víctor D. Carmona-Galindo, Claire C. Sheppard, Madelyn L. Bastin, Megan R. Kehrig, Maria F. Marín-Recinos, Joyce J. Choi and Vianney Castañeda de Abrego
Pathogens 2021, 10(6), 753; https://doi.org/10.3390/pathogens10060753 - 14 Jun 2021
Cited by 2 | Viewed by 2394
Abstract
Chagas disease is caused by the parasite Trypanosoma cruzi, which is transmitted by insect-vectors in the taxonomic subfamily Triatominae and affects approximately 8,000,000 people world-wide. Current mitigation strategies for Chagas focus on insecticides, infrastructure improvements, and management of symptoms, which are largely [...] Read more.
Chagas disease is caused by the parasite Trypanosoma cruzi, which is transmitted by insect-vectors in the taxonomic subfamily Triatominae and affects approximately 8,000,000 people world-wide. Current mitigation strategies for Chagas focus on insecticides, infrastructure improvements, and management of symptoms, which are largely unsustainable in underserved communities where the disease is widespread. Transmission patterns of vector-borne diseases are known to adaptively respond to habitat change; as such, the objective of our study was to evaluate how the physical characteristics of Triatoma dimidiata would vary in relation to land use in El Salvador. We hypothesized that the color and morphology of T. dimidiata would change with municipal levels of urban and natural green space, natural green space, and agricultural space, as well as municipal diversity, richness, and evenness of land use types. Our results characterize how T. dimidiata color and morphology vary directly with anthropogenic changes to natural and agricultural environments, which are reflective of a highly adaptable population primed to respond to environmental change. Mitigation studies of Chagas disease should exploit the relationships between anthropogenic land use and T. dimidiata morphology to evaluate how the transmission pattern of T. cruzi and Chagas disease symptomology are impacted. Full article
(This article belongs to the Special Issue Host-Pathogen Interaction Involved in Trypanosoma cruzi Infection)
24 pages, 3935 KiB  
Article
Participation of Central Muscarinic Receptors on the Nervous Form of Chagas Disease in Mice Infected via Intracerebroventricular with Colombian Trypanosoma cruzi Strain
by Gabriela Maira Pereira de Assis, Micheline Freire Donato, Matheus Marques Milagre, Samantha Ribeiro Béla, Mayra Fernanda Ricci, Luara Augusta Batista, Maria Elena de Lima, Fabrício de Araujo Moreira, Rosa Maria Esteves Arantes and Marta de Lana
Pathogens 2021, 10(2), 121; https://doi.org/10.3390/pathogens10020121 - 25 Jan 2021
Cited by 2 | Viewed by 2276
Abstract
Acute chagasic encephalitis is a clinically severe central nervous system (CNS) manifestation. However, the knowledge of the nervous form of Chagas disease is incomplete. The role of the muscarinic acetylcholine receptor (mAChR) on mice behavior and brain lesions induced by Trypanosoma cruzi (Colombian [...] Read more.
Acute chagasic encephalitis is a clinically severe central nervous system (CNS) manifestation. However, the knowledge of the nervous form of Chagas disease is incomplete. The role of the muscarinic acetylcholine receptor (mAChR) on mice behavior and brain lesions induced by Trypanosoma cruzi (Colombian strain) was herein investigated in mice treated with the mAChR agonist and antagonist (carbachol and atropine), respectively. Immunosuppressed or non-immunosuppressed mice were intracerebroventricularly (icv) or intraperitoneally (ip) infected. All groups were evaluated 15 d.p.i. (days post infection). Intraperitoneally infected animals had subpatent parasitemia. Patent parasitemia occurred only in icv infected mice. The blockade of mAChR increased the parasitemia, parasitism and lesions compared to its activation. Infected not treated (INT ip) mice did not present meningitis and encephalitis, regardless of immunosuppression. INT icv brains presented higher cellularity, discrete signs of cellular degeneration, frequent presence of parasites and focal meningitis. The immunosuppressed atropine + icv mice presented increased intracellular parasitism associated with degenerative parenchymal changes, while carbachol + icv mice presented discrete meningitis, preservation of the cortex and absence of relevant parasitism. Cholinergic receptor blockage increased impairment of coordination vs. receptor activation. Muscarinic cholinergic pathway seems to be involved in immune mediated cell invasion events while its blockade favored infection evolution, brain lesions, and behavioral alterations. Full article
(This article belongs to the Special Issue Host-Pathogen Interaction Involved in Trypanosoma cruzi Infection)
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17 pages, 2210 KiB  
Article
Triatomine Feeding Profiles and Trypanosoma cruzi Infection, Implications in Domestic and Sylvatic Transmission Cycles in Ecuador
by Sofía Ocaña-Mayorga, Juan José Bustillos, Anita G. Villacís, C. Miguel Pinto, Simone Frédérique Brenière and Mario J. Grijalva
Pathogens 2021, 10(1), 42; https://doi.org/10.3390/pathogens10010042 - 07 Jan 2021
Cited by 17 | Viewed by 3008
Abstract
Understanding the blood meal patterns of insects that are vectors of diseases is fundamental in unveiling transmission dynamics and developing strategies to impede or decrease human–vector contact. Chagas disease has a complex transmission cycle that implies interactions between vectors, parasites and vertebrate hosts. [...] Read more.
Understanding the blood meal patterns of insects that are vectors of diseases is fundamental in unveiling transmission dynamics and developing strategies to impede or decrease human–vector contact. Chagas disease has a complex transmission cycle that implies interactions between vectors, parasites and vertebrate hosts. In Ecuador, limited data on human infection are available; however, the presence of active transmission in endemic areas has been demonstrated. The aim of this study was to determine the diversity of hosts that serve as sources of blood for triatomines in domestic, peridomestic and sylvatic transmission cycles, in two endemic areas of Ecuador (central coastal and southern highland regions). Using conserved primers and DNA extracted from 507 intestinal content samples from five species of triatomines (60 Panstrongylus chinai, 17 Panstrongylus howardi, 1 Panstrongylus rufotuberculatus, 427 Rhodnius ecuadoriensis and 2 Triatoma carrioni) collected from 2006 to 2013, we amplified fragments of the cytb mitochondrial gene. After sequencing, blood meal sources were identified in 416 individuals (146 from central coastal and 270 from southern highland regions), achieving ≥ 95% identity with GenBank sequences (NCBI-BLAST tool). The results showed that humans are the main source of food for triatomines, indicating that human–vector contact is more frequent than previously thought. Although other groups of mammals, such as rodents, are also an available source of blood, birds (particularly chickens) might have a predominant role in the maintenance of triatomines in these areas. However, the diversity of sources of blood found might indicate a preference driven by triatomine species. Moreover, the presence of more than one source of blood in triatomines collected in the same place indicated that dispersal of vectors occurs regardless the availability of food. Dispersal capacity of triatomines needs to be evaluated to propose an effective strategy that limits human–vector contact and, in consequence, to decrease the risk of T. cruzi transmission. Full article
(This article belongs to the Special Issue Host-Pathogen Interaction Involved in Trypanosoma cruzi Infection)
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Review

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32 pages, 3713 KiB  
Review
Molecular and Clinical Aspects of Chronic Manifestations in Chagas Disease: A State-of-the-Art Review
by Germán J. Medina-Rincón, Sebastián Gallo-Bernal, Paula A. Jiménez, Lissa Cruz-Saavedra, Juan David Ramírez, María Juliana Rodríguez, Ramón Medina-Mur, Gustavo Díaz-Nassif, María Daniela Valderrama-Achury and Héctor M. Medina
Pathogens 2021, 10(11), 1493; https://doi.org/10.3390/pathogens10111493 - 16 Nov 2021
Cited by 11 | Viewed by 5830
Abstract
Chronic manifestations of Chagas disease present as disabling and life-threatening conditions affecting mainly the cardiovascular and gastrointestinal systems. Although meaningful research has outlined the different molecular mechanisms underlying Trypanosoma cruzi’s infection and the host-parasite interactions that follow, prompt diagnosis and treatment remain a [...] Read more.
Chronic manifestations of Chagas disease present as disabling and life-threatening conditions affecting mainly the cardiovascular and gastrointestinal systems. Although meaningful research has outlined the different molecular mechanisms underlying Trypanosoma cruzi’s infection and the host-parasite interactions that follow, prompt diagnosis and treatment remain a challenge, particularly in developing countries and also in those where the disease is considered non-endemic. This review intends to present an up-to-date review of the parasite’s life cycle, genetic diversity, virulence factors, and infective mechanisms, as well as the epidemiology, clinical presentation, diagnosis, and treatment options of the main chronic complications of Chagas disease. Full article
(This article belongs to the Special Issue Host-Pathogen Interaction Involved in Trypanosoma cruzi Infection)
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28 pages, 1723 KiB  
Review
The Liver and the Hepatic Immune Response in Trypanosoma cruzi Infection, a Historical and Updated View
by Natalia Vacani-Martins, Marcelo Meuser-Batista, Carina de Lima Pereira dos Santos, Alejandro Marcel Hasslocher-Moreno and Andrea Henriques-Pons
Pathogens 2021, 10(9), 1074; https://doi.org/10.3390/pathogens10091074 - 25 Aug 2021
Cited by 7 | Viewed by 3724
Abstract
Chagas disease was described more than a century ago and, despite great efforts to understand the underlying mechanisms that lead to cardiac and digestive manifestations in chronic patients, much remains to be clarified. The disease is found beyond Latin America, including Japan, the [...] Read more.
Chagas disease was described more than a century ago and, despite great efforts to understand the underlying mechanisms that lead to cardiac and digestive manifestations in chronic patients, much remains to be clarified. The disease is found beyond Latin America, including Japan, the USA, France, Spain, and Australia, and is caused by the protozoan Trypanosoma cruzi. Dr. Carlos Chagas described Chagas disease in 1909 in Brazil, and hepatomegaly was among the clinical signs observed. Currently, hepatomegaly is cited in most papers published which either study acutely infected patients or experimental models, and we know that the parasite can infect multiple cell types in the liver, especially Kupffer cells and dendritic cells. Moreover, liver damage is more pronounced in cases of oral infection, which is mainly found in the Amazon region. However, the importance of liver involvement, including the hepatic immune response, in disease progression does not receive much attention. In this review, we present the very first paper published approaching the liver’s participation in the infection, as well as subsequent papers published in the last century, up to and including our recently published results. We propose that, after infection, activated peripheral T lymphocytes reach the liver and induce a shift to a pro-inflammatory ambient environment. Thus, there is an immunological integration and cooperation between peripheral and hepatic immunity, contributing to disease control. Full article
(This article belongs to the Special Issue Host-Pathogen Interaction Involved in Trypanosoma cruzi Infection)
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