Special Issue "Bacterial Exotoxins and Their Impact on Host–Pathogen Interaction in Animals and Humans"

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

Deadline for manuscript submissions: 31 December 2021.

Special Issue Editor

Prof. Horst Posthaus
E-Mail Website
Guest Editor
Institute of Animal Pathology, Department of Infectious Diseases and Pathobiology, Vetsuisse Faculty, University of Bern, Switzerland
Interests: pathogenesis and pathology of bacterial infections; host-pathogen interaction; bacterial exotoxins; pore-forming toxins; clostridium perfringens toxins

Special Issue Information

Dear Colleagues,

Bacterial infections are a threat to human and animal health worldwide. In light of the increasing problem of antibiotic resistance, alternative treatments are needed. Understanding the mechanisms underlying host–pathogen interactions is crucial for the development of such alternative approaches. Many bacterial pathogens manipulate host cells and tissues via secreted toxins. A plethora of toxins targeting different cellular structures and functions has thus evolved. Toxic attacks on host cells come in many different flavors, ranging from an attack of the plasma membrane via a secreted enzyme to the internalization of multifunctional protein complexes that specifically target intracellular structures or pathways. In-depth knowledge about the mechanisms of how such specified toxins manipulate not only cellular, but also organ and body functions is central for our understanding of the pathogenesis of animal and human bacterial infections. Likewise, the host's cellular and systemic reactions to such "toxin attacks" contribute to disease and must be considered for the design of alternative treatments.

This Special Issue will focus on mechanisms of toxicity exploited by bacterial exotoxins, their effects on target cells and whole organisms as well as host reactions and defense mechanisms in response to these toxic effects. Original research articles, communications or reviews focused on these bacterial exotoxin–host interactions in animal and human disease are welcome.

Prof. Horst Posthaus
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 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

  • bacterial exotoxins
  • bacterial pathogens
  • animal
  • human
  • host–pathogen interaction
  • cellular toxicity
  • cell defense mechanisms
  • systemic effects

Published Papers (3 papers)

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Research

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Open AccessArticle
Small Pore-Forming Toxins Different Membrane Area Binding and Ca2+ Permeability of Pores Determine Cellular Resistance of Monocytic Cells
Toxins 2021, 13(2), 126; https://doi.org/10.3390/toxins13020126 - 09 Feb 2021
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Abstract
Pore-forming toxins (PFTs) form multimeric trans-membrane pores in cell membranes that differ in pore channel diameter (PCD). Cellular resistance to large PFTs (>20 nm PCD) was shown to rely on Ca2+ influx activated membrane repair mechanisms. Small PFTs (<2 nm PCD) were [...] Read more.
Pore-forming toxins (PFTs) form multimeric trans-membrane pores in cell membranes that differ in pore channel diameter (PCD). Cellular resistance to large PFTs (>20 nm PCD) was shown to rely on Ca2+ influx activated membrane repair mechanisms. Small PFTs (<2 nm PCD) were shown to exhibit a high cytotoxic activity, but host cell response and membrane repair mechanisms are less well studied. We used monocytic immune cell lines to investigate the cellular resistance and host membrane repair mechanisms to small PFTs lysenin (Eisenia fetida) and aerolysin (Aeromonas hydrophila). Lysenin, but not aerolysin, is shown to induce Ca2+ influx from the extracellular space and to activate Ca2+ dependent membrane repair mechanisms. Moreover, lysenin binds to U937 cells with higher efficiency as compared to THP-1 cells, which is in line with a high sensitivity of U937 cells to lysenin. In contrast, aerolysin equally binds to U937 or THP-1 cells, but in different plasma membrane areas. Increased aerolysin induced cell death of U937 cells, as compared to THP-1 cells, is suggested to be a consequence of cap-like aerolysin binding. We conclude that host cell resistance to small PFTs attack comprises binding efficiency, pore localization, and capability to induce Ca2+ dependent membrane repair mechanisms. Full article
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Open AccessArticle
Anthrax Edema and Lethal Toxins Differentially Target Human Lung and Blood Phagocytes
Toxins 2020, 12(7), 464; https://doi.org/10.3390/toxins12070464 - 20 Jul 2020
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Abstract
Bacillus anthracis, the causative agent of inhalation anthrax, is a serious concern as a bioterrorism weapon. The vegetative form produces two exotoxins: Lethal toxin (LT) and edema toxin (ET). We recently characterized and compared six human airway and alveolar-resident phagocyte (AARP) subsets [...] Read more.
Bacillus anthracis, the causative agent of inhalation anthrax, is a serious concern as a bioterrorism weapon. The vegetative form produces two exotoxins: Lethal toxin (LT) and edema toxin (ET). We recently characterized and compared six human airway and alveolar-resident phagocyte (AARP) subsets at the transcriptional and functional levels. In this study, we examined the effects of LT and ET on these subsets and human leukocytes. AARPs and leukocytes do not express high levels of the toxin receptors, tumor endothelium marker-8 (TEM8) and capillary morphogenesis protein-2 (CMG2). Less than 20% expressed surface TEM8, while less than 15% expressed CMG2. All cell types bound or internalized protective antigen, the common component of the two toxins, in a dose-dependent manner. Most protective antigen was likely internalized via macropinocytosis. Cells were not sensitive to LT-induced apoptosis or necrosis at concentrations up to 1000 ng/mL. However, toxin exposure inhibited B. anthracis spore internalization. This inhibition was driven primarily by ET in AARPs and LT in leukocytes. These results support a model of inhalation anthrax in which spores germinate and produce toxins. ET inhibits pathogen phagocytosis by AARPs, allowing alveolar escape. In late-stage disease, LT inhibits phagocytosis by leukocytes, allowing bacterial replication in the bloodstream. Full article
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Review

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Open AccessReview
Spatiotemporal Regulation of Vibrio Exotoxins by HlyU and Other Transcriptional Regulators
Toxins 2020, 12(9), 544; https://doi.org/10.3390/toxins12090544 - 22 Aug 2020
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Abstract
After invading a host, bacterial pathogens secrete diverse protein toxins to disrupt host defense systems. To ensure successful infection, however, pathogens must precisely regulate the expression of those exotoxins because uncontrolled toxin production squanders energy. Furthermore, inappropriate toxin secretion can trigger host immune [...] Read more.
After invading a host, bacterial pathogens secrete diverse protein toxins to disrupt host defense systems. To ensure successful infection, however, pathogens must precisely regulate the expression of those exotoxins because uncontrolled toxin production squanders energy. Furthermore, inappropriate toxin secretion can trigger host immune responses that are detrimental to the invading pathogens. Therefore, bacterial pathogens use diverse transcriptional regulators to accurately regulate multiple exotoxin genes based on spatiotemporal conditions. This review covers three major exotoxins in pathogenic Vibrio species and their transcriptional regulation systems. When Vibrio encounters a host, genes encoding cytolysin/hemolysin, multifunctional-autoprocessing repeats-in-toxin (MARTX) toxin, and secreted phospholipases are coordinately regulated by the transcriptional regulator HlyU. At the same time, however, they are distinctly controlled by a variety of other transcriptional regulators. How this coordinated but distinct regulation of exotoxins makes Vibrio species successful pathogens? In addition, anti-virulence strategies that target the coordinating master regulator HlyU and related future research directions are discussed. Full article
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