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Pathogens
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Editorial Board Members’ Collection Series: Feature Papers in Infection and...
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Editorial Board Members’ Collection Series: Feature Papers in Infection and Immunity

A special issue of Pathogens (ISSN 2076-0817). This special issue belongs to the section "Immunological Responses and Immune Defense Mechanisms".

Deadline for manuscript submissions: closed (30 November 2023) | Viewed by 8677

Special Issue Editors

Prof. Dr. Guolong Zhang

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Guest Editor
Department of Animal Science, Oklahoma State University, Stillwater, OK 74078, USA
Interests: animal innate immunity and intestinal microbiota
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Søren Skov

E-Mail Website
Guest Editor
Department of Veterinary and Animal Sciences, University of Copenhagen, 1870 Frederiksberg C, Denmark
Interests: host pathogen interaction; immunometabolism; T cell regulation and biology; macrophage regulation and biology; NK cell regulation and biology
Prof. Dr. Neil Foster

E-Mail
Guest Editor
Head of Veterinary and Animal Science, SRUC Aberdeen Campus, Craibstone Estate, Ferguson Building, Aberdeen AB21 9YA, UK
Interests: innate immune responses to microbial infections; inflammation and immunomodulation; development of biomarkers of disease
Special Issues, Collections and Topics in MDPI journals
Dr. Claudia Matteucci

E-Mail Website
Guest Editor
Department of Experimental Medicine, University of Rome Tor Vergata, Via Montpellier 1, 00133 Rome, Italy
Interests: microbiology; immunology; cancer biology; host-microbe interactions; flow cytometry; immunophenotyping; apoptosis; endogenous retroviruses; COVID-19

Special Issue Information

Dear Colleagues,

We are pleased to announce this Collection titled “Editorial Board Members’ Collection Series: Feature Papers in Infection and Immunity”, which will collect papers invited by the Editorial Board Members.

The aim of this Collection is to provide a venue for networking and communication between the journal Pathogens and scholars in the field of infection and immunity. This collection is devoted to the advancement of knowledge concerning infections caused by pathogens and immune responses to these pathogenic microorganisms, including viruses, bacteria, fungi, and parasites. Manuscripts on immunology, microbiology, infectious diseases, bacteriology, virology, mycology, and parasitology are welcome. We invite experts worldwide to submit research or review articles related to this important topic. All papers will be published open access following peer review.

Prof. Dr. Guolong Zhang
Prof. Dr. Søren Skov
Prof. Dr. Neil Foster
Dr. Claudia Matteucci
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 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

  • pathogens
  • infection
  • immunity
  • viruses
  • bacteria
  • fungi
  • parasites

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Further information on MDPI's Special Issue polices can be found here.

Published Papers (5 papers)

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Research

14 pages, 11537 KiB  
Article
A Myeloid-Specific Lack of IL-4Rα Prevents the Development of Alternatively Activated Macrophages and Enhances Immunity to Experimental Cysticercosis
by Jonadab E. Olguín, Edmundo Corano-Arredondo, Victoria Hernández-Gómez, Irma Rivera-Montoya, Mario A. Rodríguez, Itzel Medina-Andrade, Berenice Arendse, Frank Brombacher and Luis I. Terrazas
Pathogens 2024, 13(2), 169; https://doi.org/10.3390/pathogens13020169 - 13 Feb 2024
Viewed by 1328
Abstract
To determine the role that the IL-4/IL13 receptor plays in the development of alternatively activated macrophages (AAM or M2) and their role in the regulation of immunity to the extraintestinal phase of the helminth parasite Taenia crassiceps, we followed the infection in [...] Read more.
To determine the role that the IL-4/IL13 receptor plays in the development of alternatively activated macrophages (AAM or M2) and their role in the regulation of immunity to the extraintestinal phase of the helminth parasite Taenia crassiceps, we followed the infection in a mouse strain lacking the IL-4Rα gene (IL-4Rα−/−) and in the macrophage/neutrophil-specific IL-4Rα-deficient mouse strain (LysMcreIL-4Rα−/lox or cre/LoxP). While 100% of T. crassiceps-infected IL-4Rα+/+ (WT) mice harbored large parasite loads, more than 50% of th eIL-4Rα−/− mice resolved the infection. Approximately 88% of the LysMcreIL-4Rα−/lox mice displayed a sterilizing immunity to the infection. The remaining few infected cre/LoxP mice displayed the lowest number of larvae in their peritoneal cavity. The inability of the WT mice to control the infection was associated with antigen-specific Th2-type responses with higher levels of IgG1, IL-4, IL-13, and total IgE, reduced NO production, and increased arginase activity. In contrast, IL-4Rα−/− semi-resistant mice showed a Th1/Th2 combined response. Furthermore, macrophages from the WT mice displayed higher transcripts for Arginase-1 and RELM-α, as well as increased expression of PD-L2 with robust suppressive activity over anti-CD3/CD28 stimulated T cells; all of these features are associated with the AAM or M2 macrophage phenotype. In contrast, both the IL-4Rα−/− and LysMcreIL-4Rα−/lox mice did not fully develop AAM or display suppressive activity over CD3/CD28 stimulated T cells, reducing PDL2 expression. Additionally, T-CD8+ but no T-CD4+ cells showed a suppressive phenotype with increased Tim-3 and PD1 expression in WT and IL-4Rα−/−, which were absent in T. crassiceps-infected LysMcreIL-4Rα−/lox mice. These findings demonstrate a critical role for the IL-4 signaling pathway in sustaining AAM and its suppressive activity during cysticercosis, suggesting a pivotal role for AAM in favoring susceptibility to T. crassiceps infection. Thus, the absence of these suppressor cells is one of the leading mechanisms to control experimental cysticercosis successfully. Full article
(This article belongs to the Special Issue Editorial Board Members’ Collection Series: Feature Papers in Infection and Immunity)
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14 pages, 3324 KiB  
Article
HIV-Infected Hepatic Stellate Cells or HCV-Infected Hepatocytes Are Unable to Promote Latency Reversal among HIV-Infected Mononuclear Cells
by Cinthya Alicia Marcela López, Rosa Nicole Freiberger, Franco Agustín Sviercz, Jorge Quarleri and María Victoria Delpino
Pathogens 2024, 13(2), 134; https://doi.org/10.3390/pathogens13020134 - 1 Feb 2024
Cited by 1 | Viewed by 1458
Abstract
Due to a common mode of transmission through infected human blood, hepatitis C virus (HCV) and human immunodeficiency virus (HIV) co-infection is relatively prevalent. In alignment with this, HCV co-infection is associated with an increased size of the HIV reservoir in highly active [...] Read more.
Due to a common mode of transmission through infected human blood, hepatitis C virus (HCV) and human immunodeficiency virus (HIV) co-infection is relatively prevalent. In alignment with this, HCV co-infection is associated with an increased size of the HIV reservoir in highly active antiretroviral therapy (HAART)-treated individuals. Hence, it is crucial to comprehend the physiological mechanisms governing the latency and reactivation of HIV in reservoirs. Consequently, our study delves into the interplay between HCV/HIV co-infection in liver cells and its impact on the modulation of HIV latency. We utilized the latently infected monocytic cell line (U1) and the latently infected T-cell line (J-Lat) and found that mediators produced by the infection of hepatic stellate cells and hepatocytes with HIV and HCV, respectively, were incapable of inducing latency reversal under the studied conditions. This may favor the maintenance of the HIV reservoir size among latently infected mononuclear cells in the liver. Further investigations are essential to elucidate the role of the interaction between liver cells in regulating HIV latency and/or reactivation, providing a physiologically relevant model for comprehending reservoir microenvironments in vivo. Full article
(This article belongs to the Special Issue Editorial Board Members’ Collection Series: Feature Papers in Infection and Immunity)
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11 pages, 1566 KiB  
Article
HSV-1 Triggers an Antiviral Transcriptional Response during Viral Replication That Is Completely Abrogated in PKR−/− Cells
by Rosamaria Pennisi and Maria Teresa Sciortino
Pathogens 2023, 12(9), 1126; https://doi.org/10.3390/pathogens12091126 - 3 Sep 2023
Cited by 2 | Viewed by 1721
Abstract
The activation of the innate immune response during HSV-1 infection stimulates several transcription factors, such as NF-κB and IRF3, which are critical regulators of IFN-β expression. The released IFN-β activates the ISGs, which encode antiviral effectors such as the PKR. We found that [...] Read more.
The activation of the innate immune response during HSV-1 infection stimulates several transcription factors, such as NF-κB and IRF3, which are critical regulators of IFN-β expression. The released IFN-β activates the ISGs, which encode antiviral effectors such as the PKR. We found that HSV-1 triggers an antiviral transcriptional response during viral replication by activating TBK1-IRF3-NF-κB network kinetically. In contrast, we reported that infected PKR−/− cells fail to activate the transcription of TBK1. Downstream, TBK1 was unable to activate the transcription of IRF3 and NF-κB. These data suggested that in PKR−/− cells, HSV-1 replication counteracts TBK1-IRF3-NF-κB network. In this scenario, a combined approach of gene knockout and gene silencing was used to determine how the lack of PKR facilitates HSV-1 replication. We reported that in HEp-2-infected cells, PKR can influence the TBK1-IRF3-NF-κB network, consequently interfering with viral replication. Otherwise, an abrogated PKR-mediated signaling sustains the HSV-1 replication. Our result allows us to add additional information on the complex HSV-host interaction network by reinforcing the concept of the PKR role in the innate response-related networks during HSV replication in an in vitro model. Full article
(This article belongs to the Special Issue Editorial Board Members’ Collection Series: Feature Papers in Infection and Immunity)
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9 pages, 1666 KiB  
Article
Assessment of an Enterobactin Conjugate Vaccine in Layers to Protect Their Offspring from Colibacillosis
by Huiwen Wang, Catherine M. Logue, Lisa K. Nolan and Jun Lin
Pathogens 2023, 12(8), 1002; https://doi.org/10.3390/pathogens12081002 - 31 Jul 2023
Cited by 2 | Viewed by 1291
Abstract
Colibacillosis, caused by avian pathogenic Escherichia coli (APEC), is an important infectious disease in chickens and a major cause of mortality in young chicks. Therefore, protecting young chickens from colibacillosis is important for improving welfare and productivity in the poultry industry. Recently, we [...] Read more.
Colibacillosis, caused by avian pathogenic Escherichia coli (APEC), is an important infectious disease in chickens and a major cause of mortality in young chicks. Therefore, protecting young chickens from colibacillosis is important for improving welfare and productivity in the poultry industry. Recently, we developed a novel enterobactin (Ent) conjugate vaccine that could induce high titers of anti-Ent immunoglobulin Y (IgY) in chicken serum and consequently mitigate the organ lesions caused by APEC infection. Considering that maternal immunization is a practical approach to confer instant immune protection to the hatchlings, in this study, we immunized breeder hens with the Ent conjugate vaccine and evaluated the maternal immune protection on the progenies challenged with APEC. Three doses of the vaccine induced high titers of anti-Ent IgY in the hens (about 16- and 64-fold higher than the control group in the sera and egg yolks, respectively), resulting in an eight-fold of increase in anti-Ent IgY in the sera of progenies. However, the anti-Ent maternal immunity did not display significant protection against APEC challenge in the young chicks as there was no significant difference in APEC load (in liver, lung, and spleen) or organ lesions (in heart, liver, spleen, lung, and air sac) between the vaccinated and control groups. In future studies, the APEC infection model needs to be optimized to exhibit proper pathogenicity of APEC, and the maternal immunization regimen can be further improved to boost the maternally derived anti-Ent IgY in the hatchlings. Full article
(This article belongs to the Special Issue Editorial Board Members’ Collection Series: Feature Papers in Infection and Immunity)
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11 pages, 2282 KiB  
Article
NRF2 Antioxidant Response and Interferon-Stimulated Genes Are Differentially Expressed in Respiratory-Syncytial-Virus- and Rhinovirus-Infected Hospitalized Children
by Leonardo Sorrentino, Walter Toscanelli, Matteo Fracella, Marta De Angelis, Federica Frasca, Carolina Scagnolari, Laura Petrarca, Raffaella Nenna, Fabio Midulla, Anna Teresa Palamara, Lucia Nencioni and Alessandra Pierangeli
Pathogens 2023, 12(4), 577; https://doi.org/10.3390/pathogens12040577 - 9 Apr 2023
Cited by 5 | Viewed by 2217
Abstract
Respiratory diseases caused by respiratory syncytial virus (RSV) and human rhinovirus (HRV) are frequent causes of the hospitalization of children; nonetheless, RSV is responsible for the most severe and life-threatening illnesses. Viral infection triggers an inflammatory response, activating interferon (IFN)-mediated responses, including IFN-stimulated [...] Read more.
Respiratory diseases caused by respiratory syncytial virus (RSV) and human rhinovirus (HRV) are frequent causes of the hospitalization of children; nonetheless, RSV is responsible for the most severe and life-threatening illnesses. Viral infection triggers an inflammatory response, activating interferon (IFN)-mediated responses, including IFN-stimulated genes (ISG) expression with antiviral and immunomodulatory activities. In parallel, the reactive oxygen species (ROS) production activates nuclear factor erythroid 2-related factor 2 (NRF2), whose antioxidant activity can reduce inflammation by interacting with the NF-kB pathway and the IFN response. To clarify how the interplay of IFN and NRF2 may impact on clinical severity, we enrolled children hospitalized for bronchiolitis and pneumonia, and measured gene expression of type-I and III IFNs, of several ISGs, of NRF2 and antioxidant-related genes, i.e., glucose-6-phosphate dehydrogenase (G6PD), heme oxygenase 1 (HO1), and NAD(P)H dehydrogenase [Quinone] 1 (NQO1) in RSV- (RSV-A N = 33 and RSV-B N = 30) and HRV (N = 22)-positive respiratory samples. NRF2 and HO1 expression is significantly elevated in children with HRV infection compared to RSV (p = 0.012 and p = 0.007, respectively), whereas ISG15 and ISG56 expression is higher in RSV-infected children (p = 0.016 and p = 0.049, respectively). Children admitted to a pediatric intensive care unit (PICU) had reduced NRF2 expression (p = 0.002). These data suggest, for the first time, that lower activation of the NRF2 antioxidant response in RSV-infected infants may contribute to bronchiolitis severity. Full article
(This article belongs to the Special Issue Editorial Board Members’ Collection Series: Feature Papers in Infection and Immunity)
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