Toxin–Host Interaction of Clostridium Toxins: 2nd Edition

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

Deadline for manuscript submissions: 30 April 2026 | Viewed by 1003

Special Issue Editor


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Guest Editor
Institut d'Investigació Biomedica de Bellvitge, Hospitalet de Llobregat, Barcelona, Spain
Interests: bacterial protein toxins; pore-forming toxins; neurotoxins; microvesicles; exosomes; demyelinating diseases; oli-godendrocytes; glial cells; gut–brain axis; blood–brain barrier crossing; immune system; lipid rafts
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Special Issue Information

Dear Colleagues,

Following on from the first Special Issue, this Special Issue, “Toxin–Host Interaction of Clostridium Toxins: 2nd Edition”, will continue to focus on the study of the toxin–host interactions of Clostridium toxins and bring together the latest research findings in this field.

In this Special Issue, we welcome expert reviews of clinical aspects of host intoxication, as well as research papers on the following subtopics:

  • Structural studies of the toxin binding to the host cell receptor;
  • The effects of the clostridial toxins in the host cells;
  • The implication of the clostridial toxins in the gut–brain axis;
  • The effects of clostridial toxins in the blood and in the immune system;
  • New methods of toxin detection and diagnosis in host animals;
  • Novel toxin neutralizing molecules;
  • New vaccines against clostridial diseases;
  • New clostridial toxin mutants;
  • The study of clostridial toxins as therapeutic agents.

Dr. Jonatan Dorca-Arévalo
Guest Editor

Manuscript Submission Information

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Keywords

  • clostridial toxins
  • gut–brain axis
  • clostridial vaccines
  • clostridial diseases
  • clostridial toxin structure
  • clostridial toxin effects

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Published Papers (1 paper)

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Research

11 pages, 1634 KB  
Article
Botulinum Toxin Complex Serotype B-Okra Exerts Systemic Toxicity via the Oral Route by Disrupting the Intestinal Epithelial Barrier
by Chiyono Morimoto, Sho Amatsu, Takuhiro Matsumura, Masahiko Zuka and Yukako Fujinaga
Toxins 2025, 17(9), 443; https://doi.org/10.3390/toxins17090443 - 4 Sep 2025
Viewed by 659
Abstract
Botulinum toxin (BoNT) causes flaccid paralysis by blocking the release of neurotransmitters. BoNTs associate with neurotoxin-associated proteins to form medium and large progenitor toxin complexes. The large progenitor toxin complex serotype A-62A (L-PTC/A-62A) specifically targets intestinal M cells for invasion, whereas large progenitor [...] Read more.
Botulinum toxin (BoNT) causes flaccid paralysis by blocking the release of neurotransmitters. BoNTs associate with neurotoxin-associated proteins to form medium and large progenitor toxin complexes. The large progenitor toxin complex serotype A-62A (L-PTC/A-62A) specifically targets intestinal M cells for invasion, whereas large progenitor toxin complex serotype B-Okra (L-PTC/B-Okra) is mainly taken up by enterocytes and exhibits higher toxicity via the oral route. Hemagglutinin (HA) is a neurotoxin-associated protein that promotes BoNT absorption from the intestine and has carbohydrate-binding and barrier-disrupting activities. In this study, we established an in vitro reconstitution and purification system for recombinant L-PTC/B-Okra and created a recombinant L-PTC/B-Okra mutant rL-PTC/B-KA with carbohydrate-binding activity but not barrier-disrupting activity. rL-PTC/B-KA showed significantly reduced oral toxicity. Our results demonstrate that the B-Okra toxin disrupts the epithelial barrier of enterocytes and exerts oral toxicity. Full article
(This article belongs to the Special Issue Toxin–Host Interaction of Clostridium Toxins: 2nd Edition)
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