Special Issue "Effects of Microbial Toxins and Virulence Factors on Disease and Inflammation"

A special issue of Toxins (ISSN 2072-6651). This special issue belongs to the section "Bacterial Toxins".

Deadline for manuscript submissions: closed (30 September 2021).

Special Issue Editors

Dr. Laurent Boyer
E-Mail Website
Guest Editor
Inserm U1065, Université Côte d’Azur, Nice, France
Dr. Patrick Munro
E-Mail
Guest Editor
Inserm U1065, Université Côte d’Azur, Nice, France

Special Issue Information

Dear Colleagues,

Microbial toxins and virulence factors are molecular weapons used by microbes to hijack host cellular signaling pathways and increase their pathogenic potential. Different organisms use many virulence factors and toxins targeting a large array of host cell signaling pathways leading to the expression of immune responses specifically aimed toward the invading microbe. Recent findings have shown that various hosts from plant to metazoans have the ability to detect these microbial factors and mount an immune response that could be protective or detrimental if disregulated.

The aim of this Special Issue is to gather information that could expand the knowledge on the host-pathogen interaction with regards to toxins and virulence factors.  This interplay between the pathogen and its host is the focus of this monograph that intend to describe the different measures and countermeasures developed by these two partners allowing in fine to either kill the host or destroy the microbe for its own survival. We will consider original papers focusing on how toxins and virulence factors effects are favoring diseases as well as papers focusing on  how the host immunity is responding to toxins and virulence factors.  Papers adresssing these questions in various host models are welcome. Mini reviews focusing on the current knowledge of any of the mentioned topics will be also welcomed.

Dr. Laurent Boyer
Dr. Patrick Munro
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 papers will be 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 double-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Toxins 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 2400 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

  • Toxins
  • virulence factors
  • innate immunity
  • host-pathogen interactions

Published Papers (2 papers)

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Research

Article
Effect of (−)-Epigallocatechin Gallate on Activation of JAK/STAT Signaling Pathway by Staphylococcal Enterotoxin A
Toxins 2021, 13(9), 609; https://0-doi-org.brum.beds.ac.uk/10.3390/toxins13090609 - 29 Aug 2021
Viewed by 761
Abstract
Staphylococcal enterotoxin A (SEA), which is a superantigen toxin protein, binds to cytokine receptor gp130. Gp130 activates intracellular signaling pathways, including the Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway. The effects of SEA on the JAK/STAT signaling pathway in mouse spleen [...] Read more.
Staphylococcal enterotoxin A (SEA), which is a superantigen toxin protein, binds to cytokine receptor gp130. Gp130 activates intracellular signaling pathways, including the Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway. The effects of SEA on the JAK/STAT signaling pathway in mouse spleen cells were examined. After treatment with SEA, mRNA expression levels of interferon gamma (IFN-γ) and suppressor of cytokine-signaling 1 (SOCS1) increased. SEA-induced IFN-γ and SOCS1 expression were decreased by treatment with (−)-epigallocatechin gallate (EGCG). The phosphorylated STAT3, Tyr705, increased significantly in a SEA concentration-dependent manner in mouse spleen cells. Although (−)-3″-Me-EGCG did not inhibit SEA-induced phosphorylated STAT3, EGCG and (−)-4″-Me-EGCG significantly inhibited SEA-induced phosphorylated STAT3. It was thought that the hydroxyl group at position 3 of the galloyl group in the EGCG was responsible for binding to SEA and suppressing SEA-induced phosphorylation of STAT3. Through protein thermal shift assay in vitro, the binding of the gp130 receptor to SEA and the phosphorylation of STAT3 were inhibited by the interaction between EGCG and SEA. As far as we know, this is the first report to document that EGCG inhibits the binding of the gp130 receptor to SEA and the associated phosphorylation of STAT3. Full article
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Article
ClbG in Avian Pathogenic Escherichia coli Contributes to Meningitis Development in a Mouse Model
Toxins 2021, 13(8), 546; https://0-doi-org.brum.beds.ac.uk/10.3390/toxins13080546 - 06 Aug 2021
Viewed by 772
Abstract
Colibactin is a complex secondary metabolite that leads to genotoxicity that interferes with the eukaryotic cell cycle. It plays an important role in many diseases, including neonatal mouse sepsis and meningitis. Avian pathogenic Escherichia coli (APEC) is responsible for several diseases in the [...] Read more.
Colibactin is a complex secondary metabolite that leads to genotoxicity that interferes with the eukaryotic cell cycle. It plays an important role in many diseases, including neonatal mouse sepsis and meningitis. Avian pathogenic Escherichia coli (APEC) is responsible for several diseases in the poultry industry and may threaten human health due to its potential zoonosis. In this study, we confirmed that clbG was necessary for the APEC XM strain to produce colibactin. The deletion of clbG on APEC XM contributed to lowered γH2AX expression, no megalocytosis, and no cell cycle arrest in vitro. None of the 4-week Institute of Cancer Research mice infected with the APEC XM ΔclbG contracted meningitis or displayed weakened clinical symptoms. Fewer histopathological lesions were observed in the APEC XM ΔclbG group. The bacterial colonization of tissues and the relative expression of cytokines (IL-1β, IL-6, and TNF-α) in the brains decreased significantly in the APEC XM ΔclbG group compared to those in the APEC XM group. The tight junction proteins (claudin-5, occludin, and ZO-1) were not significantly destroyed in APEC XM ΔclbG group in vivo and in vitro. In conclusion, clbG is necessary for the synthesis of the genotoxin colibactin and affects the development of APEC meningitis in mice. Full article
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