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Pathogens
Special Issues
Cutting-Edge Approaches in Pathogen Study
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Cutting-Edge Approaches in Pathogen Study

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

Deadline for manuscript submissions: closed (31 December 2021) | Viewed by 17367

Special Issue Editors

Dr. Bin Gong

E-Mail Website
Guest Editor
Department of Pathology, University of Texas Medical Branch, Galveston, TX 77555, USA
Interests: microvascular dysfunction in infection and inflammation
Special Issues, Collections and Topics in MDPI journals
Dr. Tais B. Saito

E-Mail Website
Guest Editor
Division of Intramural Research, National Institute of Allergy and Infectious Diseases at the National Institute of Health, Rockville, MD 20852, USA
Interests: vector-borne diseases; immune-pathogenesis of disease; tick transmission; vector-pathogen-host interaction; immune response
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The ongoing global pandemic of the COVID-19 emphasizes again the important and emerging challenge of our times to battle dreadful pathogen-caused diseases. Nowadays, while many medical advances have been made to safeguard against infection by pathogens, through the use of vaccination, antibiotics and fungicide, pathogens continue to threaten human life. There is an urgent public health need for development of novel prophylactic and therapeutic strategies against these devastating diseases.

Research excellence in controlling pathogen-caused diseases requires use of up-to-date and standardized methodologies. Global sharing of novel technologies in the scientific community would make pathogen studies more time- and cost-effective. The aim of this Special Issue is to provide a comprehensive presentation of methodological and technological innovations in basic and clinical studies in the field of infectious diseases. The integration will allow precise characterization of pathogen-host interactions, invention of novel prophylactics and therapeutics, and advanced diagnostic methods of infectious diseases. We invite researchers interested in pathogen study to join this Special Issue and submit original research articles, short communications, and review articles for consideration. The topics cover a broad range of methods used in pathogen study including, but not limited to:

  1. Novel experimental visualizing approach；
  2. Advancement in nanotechnology combined with molecular biology for studying microorganisms associated pathogenesis, including NanoString and Nanoparticlization；
  3. Novel method for quantification of observations or improvement in quantitative method that can be employed in pathogen study； 
  4. In vitro, ex vivo, and/or in vivo research that contributes to immunotherapy, vaccination and post-exposure protection.
  5. Novel delivery modalities for prophylactic and therapeutic molecule/vaccine.

Dr. Bin Gong
Guest Editor

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.

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

Published Papers (4 papers)

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17 pages, 2872 KiB  
Article
Interaction between M. tuberculosis Lineage and Human Genetic Variants Reveals Novel Pathway Associations with Severity of TB
by Michael L. McHenry, Eddie M. Wampande, Moses L. Joloba, LaShaunda L. Malone, Harriet Mayanja-Kizza, William S. Bush, W. Henry Boom, Scott M. Williams and Catherine M. Stein
Pathogens 2021, 10(11), 1487; https://doi.org/10.3390/pathogens10111487 - 15 Nov 2021
Cited by 6 | Viewed by 3824
Abstract
Tuberculosis (TB) remains a major public health threat globally, especially in sub-Saharan Africa. Both human and Mycobacterium tuberculosis (MTBC) genetic variation affect TB outcomes, but few studies have examined if and how the two genomes interact to affect disease. We hypothesize that long-term [...] Read more.
Tuberculosis (TB) remains a major public health threat globally, especially in sub-Saharan Africa. Both human and Mycobacterium tuberculosis (MTBC) genetic variation affect TB outcomes, but few studies have examined if and how the two genomes interact to affect disease. We hypothesize that long-term coexistence between human genomes and MTBC lineages modulates disease to affect its severity. We examined this hypothesis in our TB household contact study in Kampala, Uganda, in which we identified three MTBC lineages, of which one, L4.6-Uganda, is clearly derived and hence recent. We quantified TB severity using the Bandim TBscore and examined the interaction between MTBC lineage and human single-nucleotide polymorphisms (SNPs) genome-wide, in two independent cohorts of TB cases (n = 149 and n = 127). We found a significant interaction between an SNP in PPIAP2 and the Uganda lineage (combined p = 4 × 10−8). PPIAP2 is a pseudogene that is highly expressed in immune cells. Pathway and eQTL analyses indicated potential roles between coevolving SNPs and cellular replication and metabolism as well as platelet aggregation and coagulation. This finding provides further evidence that host–pathogen interactions affect clinical presentation differently than host and pathogen genetic variation independently, and that human–MTBC coevolution is likely to explain patterns of disease severity. Full article
(This article belongs to the Special Issue Cutting-Edge Approaches in Pathogen Study)
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13 pages, 1786 KiB  
Article
Host EPAC1 Modulates Rickettsial Adhesion to Vascular Endothelial Cells via Regulation of ANXA2 Y23 Phosphorylation
by Zhengchen Su, Thomas R. Shelite, Yuan Qiu, Qing Chang, Maki Wakamiya, Jiani Bei, Xi He, Changcheng Zhou, Yakun Liu, Emmanuel Nyong, Yuejin Liang, Angelo Gaitas, Tais B. Saito and Bin Gong
Pathogens 2021, 10(10), 1307; https://doi.org/10.3390/pathogens10101307 - 12 Oct 2021
Cited by 5 | Viewed by 2862
Abstract
Introduction: Intracellular cAMP receptor exchange proteins directly activated by cAMP 1 (EPAC1) regulate obligate intracellular parasitic bacterium rickettsial adherence to and invasion into vascular endothelial cells (ECs). However, underlying precise mechanism(s) remain unclear. The aim of the study is to dissect [...] Read more.
Introduction: Intracellular cAMP receptor exchange proteins directly activated by cAMP 1 (EPAC1) regulate obligate intracellular parasitic bacterium rickettsial adherence to and invasion into vascular endothelial cells (ECs). However, underlying precise mechanism(s) remain unclear. The aim of the study is to dissect the functional role of the EPAC1-ANXA2 signaling pathway during initial adhesion of rickettsiae to EC surfaces. Methods: In the present study, an established system that is anatomically based and quantifies bacterial adhesion to ECs in vivo was combined with novel fluidic force microscopy (FluidFM) to dissect the functional role of the EPAC1-ANXA2 signaling pathway in rickettsiae–EC adhesion. Results: The deletion of the EPAC1 gene impedes rickettsial binding to endothelium in vivo. Rickettsial OmpB shows a host EPAC1-dependent binding strength on the surface of a living brain microvascular EC (BMEC). Furthermore, ectopic expression of phosphodefective and phosphomimic mutants replacing tyrosine (Y) 23 of ANXA2 in ANXA2-knock out BMECs results in different binding force to reOmpB in response to the activation of EPAC1. Conclusions: EPAC1 modulates rickettsial adhesion, in association with Y23 phosphorylation of the binding receptor ANXA2. Underlying mechanism(s) should be further explored to delineate the accurate role of cAMP-EPAC system during rickettsial infection. Full article
(This article belongs to the Special Issue Cutting-Edge Approaches in Pathogen Study)
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19 pages, 10255 KiB  
Article
Cell-Type Apoptosis in Lung during SARS-CoV-2 Infection
by Yakun Liu, Tania M. Garron, Qing Chang, Zhengchen Su, Changcheng Zhou, Yuan Qiu, Eric C. Gong, Junying Zheng, Y. Whitney Yin, Thomas Ksiazek, Trevor Brasel, Yang Jin, Paul Boor, Jason E. Comer and Bin Gong
Pathogens 2021, 10(5), 509; https://doi.org/10.3390/pathogens10050509 - 23 Apr 2021
Cited by 40 | Viewed by 7683
Abstract
The SARS-CoV-2 pandemic has inspired renewed interest in understanding the fundamental pathology of acute respiratory distress syndrome (ARDS) following infection. However, the pathogenesis of ARDS following SRAS-CoV-2 infection remains largely unknown. In the present study, we examined apoptosis in postmortem lung sections from [...] Read more.
The SARS-CoV-2 pandemic has inspired renewed interest in understanding the fundamental pathology of acute respiratory distress syndrome (ARDS) following infection. However, the pathogenesis of ARDS following SRAS-CoV-2 infection remains largely unknown. In the present study, we examined apoptosis in postmortem lung sections from COVID-19 patients and in lung tissues from a non-human primate model of SARS-CoV-2 infection, in a cell-type manner, including type 1 and 2 alveolar cells and vascular endothelial cells (ECs), macrophages, and T cells. Multiple-target immunofluorescence assays and Western blotting suggest both intrinsic and extrinsic apoptotic pathways are activated during SARS-CoV-2 infection. Furthermore, we observed that SARS-CoV-2 fails to induce apoptosis in human bronchial epithelial cells (i.e., BEAS2B cells) and primary human umbilical vein endothelial cells (HUVECs), which are refractory to SARS-CoV-2 infection. However, infection of co-cultured Vero cells and HUVECs or Vero cells and BEAS2B cells with SARS-CoV-2 induced apoptosis in both Vero cells and HUVECs/BEAS2B cells but did not alter the permissiveness of HUVECs or BEAS2B cells to the virus. Post-exposure treatment of the co-culture of Vero cells and HUVECs with a novel non-cyclic nucleotide small molecule EPAC1-specific activator reduced apoptosis in HUVECs. These findings may help to delineate a novel insight into the pathogenesis of ARDS following SARS-CoV-2 infection. Full article
(This article belongs to the Special Issue Cutting-Edge Approaches in Pathogen Study)
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Other

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14 pages, 1349 KiB  
Study Protocol
Indwelling Device-Associated Biofilms in Critically Ill Cancer Patients—Study Protocol
by Olguta Lungu, Ioana Grigoras, Olivia Simona Dorneanu, Catalina Lunca, Teodora Vremera, Stefania Brandusa Copacianu, Iuliu Ivanov and Luminita Smaranda Iancu
Pathogens 2021, 10(3), 306; https://doi.org/10.3390/pathogens10030306 - 6 Mar 2021
Cited by 1 | Viewed by 2210
Abstract
Health care-associated infections are a leading cause of inpatient complications. Rapid pathogen detection/identification is a major challenge in sepsis management that highly influences the successful outcome. The current standard of microorganism identification relies on bacterial growth in culture, which has several limitations. Gene [...] Read more.
Health care-associated infections are a leading cause of inpatient complications. Rapid pathogen detection/identification is a major challenge in sepsis management that highly influences the successful outcome. The current standard of microorganism identification relies on bacterial growth in culture, which has several limitations. Gene sequencing research has developed culture-independent techniques for microorganism identification, with the aim to improve etiological diagnosis and, therefore, to change sepsis outcome. A prospective, observational, non-interventional, single-center study was designed that assesses biofilm-associated pathogens in a specific subpopulation of septic critically ill cancer patients. Indwelling device samples will be collected in septic patients at the moment of the removal of the arterial catheter, central venous catheter, endotracheal tube and urinary catheter. Concomitantly, clinical data regarding 4 sites (nasal, pharyngeal, rectal and skin) of pathogen colonization at the time of hospital/intensive care admission will be collected. The present study aims to offer new insights into biofilm-associated infections and to evaluate the infection caused by catheter-specific and patient-specific biofilm-associated pathogens in association with the extent of colonization. The analysis relies on the two following detection/identification techniques: standard microbiological method and next generation sequencing (NGS). Retrospectively, the study will estimate the clinical value of the NGS-based detection and its virtual potential in changing patient management and outcome, notably in the subjects with missing sepsis source or lack of response to anti-infective treatment. Full article
(This article belongs to the Special Issue Cutting-Edge Approaches in Pathogen Study)
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