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Pathogens
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Mechanisms of Gene Expression Regulation during Host-Pathogen Interaction
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Mechanisms of Gene Expression Regulation during Host-Pathogen Interaction

A special issue of Pathogens (ISSN 2076-0817).

Deadline for manuscript submissions: closed (30 November 2023) | Viewed by 8060

Special Issue Editors

Dr. Jaeson Calla

E-Mail Website
Guest Editor
1. Assistant Project Scientist, School of Medicine, University of California San Diego (UCSD), San Diego, CA, USA
2. Principal Investigator, Department of Cellular and Molecular Sciences, Faculty of Sciences and Philosophy, Universidad Peruana Cayetano Heredia (UPCH), Lima, Peru
Interests: infectious disease; malaria; molecular biology; host-pathogen interactions; antimalarial drug discovery
Prof. Dr. Rossana Arroyo

E-Mail Website
Guest Editor
Departamento de Infectómica y Patogénesis Molecular, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional (CINVESTAV), Mexico City, Mexico
Interests: molecular pathogenesis; molecular biology; Trichomonas vaginalis; postranscriptional regulation by iron; glucose modulation

Special Issue Information

Dear Colleagues,

Host–pathogen interaction is complex and triggers a change in gene expression in both organisms; the mechanisms associated with the gene regulation involve dynamic changes under control: transcriptional, post-transcriptional, translational, and or post-translational levels.

In this Special Issue, we are interested in describing how unicellular or pluricellular pathogens interact, adhere, internalize, colonize, establish, multiply, and egress to infect a new cell host during a successful infection, elucidating different gene-regulation mechanisms. These can then be used to identify targets in the development of new biomolecules which could block a specific mechanism and provide an anti-pathogenic effect, which could help to eradicate or eliminate individual pathogens.

The identification of target genes and proteins would help us to develop new compounds to prevent infection (prophylactic activity), eliminate the infectious agent (therapeutic activity), or even bring new strategies to develop ways to prevent infections (like vaccines).

We invite researchers who work with infectious disease pathogens to send us their research results elucidating host–pathogen interaction mechanisms and identifying target molecules to search for new drugs for different pathogens as well as new strategies to develop vaccines.

Dr. Jaeson Calla
Prof. Dr. Rossana Arroyo
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

  • host–pathogen interactions
  • gene regulation
  • pathogenesis
  • compounds
  • drugs
  • vaccines

Published Papers (5 papers)

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Research

18 pages, 3390 KiB  
Article
The Non-Canonical Iron-Responsive Element of IRE-tvcp12 Hairpin Structure at the 3′-UTR of Trichomonas vaginalis TvCP12 mRNA That Binds TvHSP70 and TvACTN-3 Can Regulate mRNA Stability and Amount of Protein
by Claudia R. León-Sicairos, Elisa E. Figueroa-Angulo, Jaeson S. Calla-Choque and Rossana Arroyo
Pathogens 2023, 12(4), 586; https://doi.org/10.3390/pathogens12040586 - 12 Apr 2023
Cited by 1 | Viewed by 1291
Abstract
Trichomonas vaginalis is one of the most common sexually transmitted parasites in humans. This protozoan has high iron requirements for growth, metabolism, and virulence. However, iron concentrations also differentially modulate T. vaginalis gene expression as in the genes encoding cysteine proteinases TvCP4 and [...] Read more.
Trichomonas vaginalis is one of the most common sexually transmitted parasites in humans. This protozoan has high iron requirements for growth, metabolism, and virulence. However, iron concentrations also differentially modulate T. vaginalis gene expression as in the genes encoding cysteine proteinases TvCP4 and TvCP12. Our goal was to identify the regulatory mechanism mediating the upregulation of tvcp12 under iron-restricted (IR) conditions. Here, we showed by RT-PCR, Western blot, and immunocytochemistry assays that IR conditions increase mRNA stability and amount of TvCP12. RNA electrophoretic mobility shift assay (REMSA), UV cross-linking, and competition assays demonstrated that a non-canonical iron-responsive element (IRE)-like structure at the 3′-untranslated region of the tvcp12 transcript (IRE-tvcp12) specifically binds to human iron regulatory proteins (IRPs) and to atypical RNA-binding cytoplasmic proteins from IR trichomonads, such as HSP70 and α-Actinin 3. These data were confirmed by REMSA supershift and Northwestern blot assays. Thus, our findings show that a positive gene expression regulation under IR conditions occurs at the posttranscriptional level possibly through RNA-protein interactions between atypical RNA-binding proteins and non-canonical IRE-like structures at the 3′-UTR of the transcript by a parallel mechanism to the mammalian IRE/IRP system that can be applied to other iron-regulated genes of T. vaginalis. Full article
(This article belongs to the Special Issue Mechanisms of Gene Expression Regulation during Host-Pathogen Interaction)
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22 pages, 2893 KiB  
Article
Attenuation of In Vitro and In Vivo Virulence Is Associated with Repression of Gene Expression of AIG1 Gene in Entamoeba histolytica
by Janeth Lozano-Mendoza, Fátima Ramírez-Montiel, Ángeles Rangel-Serrano, Itzel Páramo-Pérez, Claudia Leticia Mendoza-Macías, Faridi Saavedra-Salazar, Bernardo Franco, Naurú Vargas-Maya, Ghulam Jeelani, Yumiko Saito-Nakano, Fernando Anaya-Velázquez, Tomoyoshi Nozaki and Felipe Padilla-Vaca
Pathogens 2023, 12(3), 489; https://doi.org/10.3390/pathogens12030489 - 21 Mar 2023
Cited by 1 | Viewed by 1643
Abstract
Entamoeba histolytica virulence results from complex host–parasite interactions implicating multiple amoebic components (e.g., Gal/GalNAc lectin, cysteine proteinases, and amoebapores) and host factors (microbiota and immune response). UG10 is a strain derived from E. histolytica virulent HM-1:IMSS strain that has lost its virulence in [...] Read more.
Entamoeba histolytica virulence results from complex host–parasite interactions implicating multiple amoebic components (e.g., Gal/GalNAc lectin, cysteine proteinases, and amoebapores) and host factors (microbiota and immune response). UG10 is a strain derived from E. histolytica virulent HM-1:IMSS strain that has lost its virulence in vitro and in vivo as determined by a decrease of hemolytic, cytopathic, and cytotoxic activities, increased susceptibility to human complement, and its inability to form liver abscesses in hamsters. We compared the transcriptome of nonvirulent UG10 and its parental HM-1:IMSS strain. No differences in gene expression of the classical virulence factors were observed. Genes downregulated in the UG10 trophozoites encode for proteins that belong to small GTPases, such as Rab and AIG1. Several protein-coding genes, including iron-sulfur flavoproteins and heat shock protein 70, were also upregulated in UG10. Overexpression of the EhAIG1 gene (EHI_180390) in nonvirulent UG10 trophozoites resulted in augmented virulence in vitro and in vivo. Cocultivation of HM-1:IMSS with E. coli O55 bacteria cells reduced virulence in vitro, and the EhAIG1 gene expression was downregulated. In contrast, virulence was increased in the monoxenic strain UG10, and the EhAIG1 gene expression was upregulated. Therefore, the EhAIG1 gene (EHI_180390) represents a novel virulence determinant in E. histolytica. Full article
(This article belongs to the Special Issue Mechanisms of Gene Expression Regulation during Host-Pathogen Interaction)
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14 pages, 2155 KiB  
Article
Lysine Methyltransferase EhPKMT2 Is Involved in the In Vitro Virulence of Entamoeba histolytica
by Susana Munguía-Robledo, Esther Orozco, Guillermina García-Rivera, Jeni Bolaños, Jesús Valdés, Elisa Azuara-Licéaga and Mario Alberto Rodríguez
Pathogens 2023, 12(3), 474; https://doi.org/10.3390/pathogens12030474 - 17 Mar 2023
Viewed by 1470
Abstract
Lysine methylation, a posttranslational modification catalyzed by protein lysine methyltransferases (PKMTs), is involved in epigenetics and several signaling pathways, including cell growth, cell migration and stress response, which in turn may participate in virulence of protozoa parasites. Entamoeba histolytica, the etiologic agent [...] Read more.
Lysine methylation, a posttranslational modification catalyzed by protein lysine methyltransferases (PKMTs), is involved in epigenetics and several signaling pathways, including cell growth, cell migration and stress response, which in turn may participate in virulence of protozoa parasites. Entamoeba histolytica, the etiologic agent of human amebiasis, has four PKMTs (EhPKMT1 to EhPKMT4), but their role in parasite biology is unknown. Here, to obtain insight into the role of EhPKMT2, we analyzed its expression level and localization in trophozoites subjected to heat shock and during phagocytosis, two events that are related to amoeba virulence. Moreover, the effect of EhPKMT2 knockdown on those activities and on cell growth, migration and cytopathic effect was investigated. The results indicate that this enzyme participates in all these cellular events, suggesting that it could be a potential target for development of novel therapeutic strategies against amebiasis. Full article
(This article belongs to the Special Issue Mechanisms of Gene Expression Regulation during Host-Pathogen Interaction)
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20 pages, 3565 KiB  
Article
A Putative New Role of Tv-PSP1 Recognizes IRE and ERE Hairpin Structures from Trichomonas vaginalis
by César Millán-Pacheco, Rodrigo Arreola, Alma Villalobos-Osnaya, Georgina Garza-Ramos, Iris N. Serratos, Adelaida Díaz-Vilchis, Enrique Rudiño-Piñera and María Elizbeth Alvarez-Sanchez
Pathogens 2023, 12(1), 79; https://doi.org/10.3390/pathogens12010079 - 03 Jan 2023
Viewed by 1315
Abstract
To understand whether protein Tv-PSP1 from Trichomonas vaginalis recognizes mRNA parasite stem-loop structures, we conducted REMSA and intrinsic fluorescence assays. We found the recombinant Tv-PSP1 structure, determined with X-ray crystallography, showed unusual thermal stability of the quaternary structure, associated with a disulfide bridge [...] Read more.
To understand whether protein Tv-PSP1 from Trichomonas vaginalis recognizes mRNA parasite stem-loop structures, we conducted REMSA and intrinsic fluorescence assays. We found the recombinant Tv-PSP1 structure, determined with X-ray crystallography, showed unusual thermal stability of the quaternary structure, associated with a disulfide bridge CYS76-CYS104. To gain deeper insight into the Tv-PSP1 interaction with mRNA stem-loops (mRNAsl) and its relationship with thermal stability, we also used an integrated computational protocol that combined molecular dynamics simulations, docking assays, and binding energy calculations. Docking models allowed us to determine a putative contact surface interaction region between Tv-PSP1 and mRNAsl. We determined the contributions of these complexes to the binding free energy (ΔGb) in the electrostatic (ΔGelec) and nonelectrostatic (ΔGnon-elec) components using the Adaptive Poisson–Boltzmann Solver (APBS) program. We are the first, to the best of our knowledge, to show the interaction between Tv-PSP1 and the stem-loop structures of mRNA. Full article
(This article belongs to the Special Issue Mechanisms of Gene Expression Regulation during Host-Pathogen Interaction)
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16 pages, 1316 KiB  
Article
CD4+ T Cell Regulatory Network Underlies the Decrease in Th1 and the Increase in Anergic and Th17 Subsets in Severe COVID-19
by Mariana Esther Martinez-Sánchez, José Alberto Choreño-Parra, Elena R. Álvarez-Buylla, Joaquín Zúñiga and Yalbi Itzel Balderas-Martínez
Pathogens 2023, 12(1), 18; https://doi.org/10.3390/pathogens12010018 - 22 Dec 2022
Viewed by 1476
Abstract
In this model we use a dynamic and multistable Boolean regulatory network to provide a mechanistic explanation of the lymphopenia and dysregulation of CD4+ T cell subsets in COVID-19 and provide therapeutic targets. Using a previous model, the cytokine micro-environments found in mild, [...] Read more.
In this model we use a dynamic and multistable Boolean regulatory network to provide a mechanistic explanation of the lymphopenia and dysregulation of CD4+ T cell subsets in COVID-19 and provide therapeutic targets. Using a previous model, the cytokine micro-environments found in mild, moderate, and severe COVID-19 with and without TGF-β and IL-10 was we simulated. It shows that as the severity of the disease increases, the number of antiviral Th1 cells decreases, while the the number of Th1-like regulatory and exhausted cells and the proportion between Th1 and Th1R cells increases. The addition of the regulatory cytokines TFG-β and IL-10 makes the Th1 attractor unstable and favors the Th17 and regulatory subsets. This is associated with the contradictory signals in the micro-environment that activate SOCS proteins that block the signaling pathways. Furthermore, it determined four possible therapeutic targets that increase the Th1 compartment in severe COVID-19: the activation of the IFN-γ pathway, or the inhibition of TGF-β or IL-10 pathways or SOCS1 protein; from these, inhibiting SOCS1 has the lowest number of predicted collateral effects. Finally, a tool is provided that allows simulations of specific cytokine environments and predictions of CD4 T cell subsets and possible interventions, as well as associated secondary effects. Full article
(This article belongs to the Special Issue Mechanisms of Gene Expression Regulation during Host-Pathogen Interaction)
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