Host–Pathogen Interactions and Their Impact on Bacterial Virulence

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

Deadline for manuscript submissions: closed (20 May 2021) | Viewed by 9540

Special Issue Editors


E-Mail Website
Guest Editor
MICALIS Institute, National Research Institute for Agriculture, Food and Environment (INRAe), University of Paris-Saclay, Jouy-en-Josas, France
Interests: foodborne pathogens; bacterial pathogenicity; host–pathogen interaction; antimicrobial; toxins

E-Mail Website
Guest Editor
IRSD, Université de Toulouse, INSERM, INRAE, ENVT, UPS, 31024 Toulouse, France
Interests: Enterobacteriaceae; genetic diversity; gene function; genomic evolution; host-pathogen interactions; ecological niche
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
UMR0454 MEDIS, National Research Institute for Agriculture, Food and Environment (INRAe), University of Clermont Auvergne, Clermont-Ferrand, France
Interests: pathogenic or commensal E. coli; virulence factors; toxins; gene regulation; E. coli interactions with the host or the gut microbiota
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Institute of Medical Microbiology, University of Zürich, Gloriastrasse 28 - 8006 Zürich, Switzerland
Interests: persistence; eco-pathology; phenotypic heterogeneity; bacterial pathogens; amoebae; infectious disease

Special Issue Information

Dear Colleagues,

We are constantly exposed to a myriad of potential pathogens through ingestion, inhalation, and contact with biotic or abiotic surfaces. Although various pathogens disseminate through human-to-human transmission, major infectious agents are often directly acquired from their environmental niches. Pathogens’ reservoirs may thus represent a training ground shaping the bacterial genome and the virulence toolkits and positively selecting for transmission and virulence traits detrimental to humans.

During the course of infection, the pathogen’s survival and proliferation relies on its ability to cope with distinct, structured, dynamic, heterogeneous, and hostile microenvironments, for which a degree of tropisms may be observed. Microbes synchronize the expression and production of virulence factors when needed during infection by responding to host-derived environmental cues and stress. Pathogens have also evolved elaborate strategies to bypass the anti-bacterial activities of the host immune system, which play decisive roles in their abilities to cause diseases.

One aspect of the complex interplay between the pathogen and the host is the production of a multitude of genetically identical individuals with distinct features. This reversible phenomenon termed “phenotypic heterogeneity” allows the microorganisms to function at a population level to support the colonization of heterogeneous environments. It is also of major clinical importance, as it involves the development of persister cells that transiently display phenotypic tolerance to antibiotic treatments, causing delays in treatments as well as persistent and relapsing infections.

Many severe bacterial infections are hard to cure even when promptly diagnosed and treated with the right antibiotics. Therapy failure partly originates from the worrisome increase in antibiotic resistance. The comprehensive understanding of the infection process may foster the identification of druggable targets and the development of effective therapeutic alternatives.

The aim of this research topic is to provide insight into the complex communication between bacterial pathogens and their host(s). More specifically, we wish to highlight how bacteria exploit host-derived cues and stress to favor increased virulence towards humans.

We seek Original Research articles, Reviews, Brief Research Reports, and Mini Reviews that cover, but are not limited to, the following topics:

  1. Resistance to and evasion of the host immune response;
  2. Bacterial transmission and adaptation to the host;
  3. The regulation of virulence programs by host signals;
  4. Bacterial phenotypic heterogeneity and persistence within the host.

Dr. Seav-ly Tran
Dr. Priscilla Branchu
Dr. Grégory Jubelin
Dr. Nicolas Personnic
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
  • stress
  • cues and adaptation
  • immune resistance
  • phenotypic heterogeneity and persistence
  • virulence gene expression

Published Papers (2 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Research

Jump to: Review

19 pages, 1151 KiB  
Article
Alpha Enolase 1 Ubiquitination and Degradation Mediated by Ehrlichia chaffeensis TRP120 Disrupts Glycolytic Flux and Promotes Infection
by Bing Zhu and Jere W. McBride
Pathogens 2021, 10(8), 962; https://doi.org/10.3390/pathogens10080962 - 30 Jul 2021
Cited by 4 | Viewed by 2315
Abstract
Ehrlichia chaffeensis modulates numerous host cell processes, including gene transcription to promote infection of the mononuclear phagocyte. Modulation of these host cell processes is directed through E. chaffeensis effectors, including TRP120. We previously reported that TRP120 moonlights as a HECT E3 Ub ligase [...] Read more.
Ehrlichia chaffeensis modulates numerous host cell processes, including gene transcription to promote infection of the mononuclear phagocyte. Modulation of these host cell processes is directed through E. chaffeensis effectors, including TRP120. We previously reported that TRP120 moonlights as a HECT E3 Ub ligase that ubiquitinates host cell transcription and fate regulators (PCGF5 and FBW7) to promote infection. In this study, we identified a novel TRP120 substrate and examined the relationship between TRP120 and α-enolase (ENO1), a metalloenzyme that catalyzes glycolytic pathway substrate dehydration. Immunofluorescence microscopy and coimmunoprecipitation demonstrated interaction between ENO1 and TRP120, and ubiquitination of ENO-1 by TRP120 was detected in vivo and in vitro. Further, ENO-1 degradation was observed during infection and was inhibited by the proteasomal inhibitor bortezomib. A direct role of TRP120 Ub ligase activity in ENO-1 degradation was demonstrated and confirmed by ectopic expression of TRP120 HECT Ub ligase catalytic site mutant. siRNA knockdown of ENO-1 coincided with increased E. chaffeensis infection and ENO-1 knockdown disrupted glycolytic flux by decreasing the levels of pyruvate and lactate that may contribute to changes in host cell metabolism that promote infection. In addition, we elucidated a functional role of TRP120 auto-ubiquitination as an activating event that facilitates the recruitment of the UbcH5 E2 ubiquitin-conjugating enzyme. This investigation further expands the repertoire of TRP120 substrates and extends the potential role of TRP120 Ub ligase in infection to include metabolic reprogramming. Full article
(This article belongs to the Special Issue Host–Pathogen Interactions and Their Impact on Bacterial Virulence)
Show Figures

Figure 1

Review

Jump to: Research

25 pages, 1303 KiB  
Review
Bacteria and Host Interplay in Staphylococcus aureus Septic Arthritis and Sepsis
by Tao Jin, Majd Mohammad, Rille Pullerits and Abukar Ali
Pathogens 2021, 10(2), 158; https://doi.org/10.3390/pathogens10020158 - 3 Feb 2021
Cited by 36 | Viewed by 6126
Abstract
Staphylococcus aureus (S. aureus) infections are a major healthcare challenge and new treatment alternatives are needed. S. aureus septic arthritis, a debilitating joint disease, causes permanent joint dysfunction in almost 50% of the patients. S. aureus bacteremia is associated with higher [...] Read more.
Staphylococcus aureus (S. aureus) infections are a major healthcare challenge and new treatment alternatives are needed. S. aureus septic arthritis, a debilitating joint disease, causes permanent joint dysfunction in almost 50% of the patients. S. aureus bacteremia is associated with higher mortalities than bacteremia caused by most other microbes and can develop to severe sepsis and death. The key to new therapies is understanding the interplay between bacterial virulence factors and host immune response, which decides the disease outcome. S. aureus produces numerous virulence factors that facilitate bacterial dissemination, invasion into joint cavity, and cause septic arthritis. Monocytes, activated by several components of S. aureus such as lipoproteins, are responsible for bone destructions. In S. aureus sepsis, cytokine storm induced by S. aureus components leads to the hyperinflammatory status, DIC, multiple organ failure, and later death. The immune suppressive therapies at the very early time point might be protective. However, the timing of treatment is crucial, as late treatment may aggravate the immune paralysis and lead to uncontrolled infection and death. Full article
(This article belongs to the Special Issue Host–Pathogen Interactions and Their Impact on Bacterial Virulence)
Show Figures

Figure 1

Back to TopTop