Special Issue "Toxins Secretion and Translocation"

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

Deadline for manuscript submissions: closed (31 May 2019).

Special Issue Editors

Guest Editor
Prof. Dr. Holger Barth E-Mail
Institut für Pharmakologie und Toxikologie, Universitätsklinikum Ulm, Albert-Einstein-Allee 11, 89081 Ulm, Germany
Phone: ++49 731 500 65503
Fax: +49 731 50065502
Interests: bacterial protein toxins; actin; Rho-GTPases; macrophages; cellular uptake and intracellular membrane transport of bacterial toxins; interaction of bacterial toxins with host cell chaperones; bacterial toxins as Molecular Trojan Horses for drug delivery
Guest Editor
Dr. Panagiotis Papatheodorou E-Mail
Institut für Pharmazeutische Biotechnologie, Universität Ulm, Institut für Pharmakologie und Toxikologie, Universitätsklinikum Ulm, Albert-Einstein-Allee 11, 89081 Ulm, Germany
Phone: +49(0)162-7837882
Interests: Clostridium difficile, clostridial toxin, bacterial toxin, toxin receptor, toxin uptake

Special Issue Information

Dear Colleagues,

Exotoxins are proteins that are produced and secreted by living bacteria. The exotoxins must be transported across one membrane in the case of Gram-positive and across two membranes in case of Gram-negative bacteria by sophisticated mechanisms in order to be released from the producing bacteria and to exhibit their cytotoxic effects on target cells. AB-type exotoxins act inside their target cells, i.e. the proteins must again cross at least one membrane barrier. To this end, AB-toxins hijack protein trafficking pathways and mechanisms of their host cells, incuding the endocytic machinery and in some cases also host cell chaperone macheries to deliver their enzymatically active (A) subunit into the cytosol. The intracellular trans-membrane transport of many toxins includes pore formation in cell membranes, which serve as translocation channels for the enzyme subunits of the toxins. This Special Issue will focus on the molecular mechanisms underlying the transport of protein toxins across membrane barriers. This includes trans-membrane transport during toxin secretion from the producing organisms, as well as the intracellular trans-membrane transport of toxins in mammalian target cells.

Prof. Dr. Holger Barth
Dr. Panagiotis Papatheodorou
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 1800 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
  • membrane transport
  • toxin secretion
  • trans-membrane pores
  • toxin translocation in host cells

Published Papers (1 paper)

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Research

Open AccessArticle
Toxin B Variants from Clostridium difficile Strains VPI 10463 and NAP1/027 Share Similar Substrate Profile and Cellular Intoxication Kinetics but Use Different Host Cell Entry Factors
Toxins 2019, 11(6), 348; https://doi.org/10.3390/toxins11060348 - 17 Jun 2019
Abstract
Clostridium difficile induces antibiotic-associated diarrhea due to the release of toxin A (TcdA) and toxin B (TcdB), the latter being its main virulence factor. The epidemic strain NAP1/027 has an increased virulence attributed to different factors. We compared cellular intoxication by TcdBNAP1 [...] Read more.
Clostridium difficile induces antibiotic-associated diarrhea due to the release of toxin A (TcdA) and toxin B (TcdB), the latter being its main virulence factor. The epidemic strain NAP1/027 has an increased virulence attributed to different factors. We compared cellular intoxication by TcdBNAP1 with that by the reference strain VPI 10463 (TcdBVPI). In a mouse ligated intestinal loop model, TcdBNAP1 induced higher neutrophil recruitment, cytokine release, and epithelial damage than TcdBVPI. Both toxins modified the same panel of small GTPases and exhibited similar in vitro autoprocessing kinetics. On the basis of sequence variations in the frizzled-binding domain (FBD), we reasoned that TcdBVPI and TcdBNAP1 might have different receptor specificities. To test this possibility, we used a TcdB from a NAP1 variant strain (TcdBNAP1v) unable to glucosylate RhoA but with the same receptor-binding domains as TcdBNAP1. Cells were preincubated with TcdBNAP1v to block cellular receptors, prior to intoxication with either TcdBVPI or TcdBNAP1. Preincubation with TcdBNAP1v blocked RhoA glucosylation by TcdBNAP1 but not by TcdBVPI, indicating that the toxins use different host factors for cell entry. This crucial difference might explain the increased biological activity of TcdBNAP1 in the intestine, representing a contributing factor for the increased virulence of the NAP1/027 strain. Full article
(This article belongs to the Special Issue Toxins Secretion and Translocation)
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