Special Issue "Enterotoxins and Mucosal Pathomechanisms"

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

Deadline for manuscript submissions: 15 August 2023 | Viewed by 1706

Special Issue Editor

Inst. Clinical Physiology / Nutritional Medicine, Dept. Gastroenterology, Charité – Universitätsmedizin Berlin, Berlin, Germany
Interests: gut pathogens; epithelial barrier function; tight junction regulation; clostridial toxins; bacterial pore-forming toxins and toxic metabolites; campylobacter toxins; colonization; invasion; leaky gut phenomenon; immune cell—epithelial cell co-culture and organoids; barrier-breaking mechanisms of arcobacter; aeromonas; campylobacter; clostridioides difficile; escherichia coli; klebisella oxytoca; salmonella; yersinia enterocoltitica; helicobacter pylori
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Special Issue Information

Dear Colleagues,

The mechanisms leading to diarrhea and inflammation in the intestinal mucosa are frequently directly caused by enterotoxins from microorganisms such as bacteria, cyanobacteria, protists, yeasts, algae or fungal toxins. Some toxins are even described to possess carcinogenic properties or genotoxic effects.

Between mild cytoskeletal alterations and rapid lethal cytotoxicity, a variety of cytopathic effects on intestinal cellular dysregulation can occur.

The topics of this Special Issue comprise insights into toxin-mediated epithelial perturbation in the gut mucosa and the inherent signaling.

Despite the description of many enterotoxins, knowledge is still lacking regarding the pathomechanisms responsible for mucosal damage and diarrhea. The diarrheal mechanisms of enterotoxins often comprise the secretory or malabsorptive type of diarrhea by the dysregulation of transporters, but also epithelial barrier dysfunction via the leak flux pathomechanism, mainly by tight junction dysregulation.

Concomitantly, the influx of noxious agents from the gut lumen can induce and aggravate mucosal inflammation, described as the leaky gut phenomenon in different inflammatory intestinal diseases. Intestinal bacterial antigens and toxins play a pivotal role in this induction of epithelial barrier dysfunction and mucosal inflammation.

Mechanisms by which toxins cross the mucosal barrier via the paracellular route or bind to cellular receptors and then take the transcellular pathway via endocytosis to gain access to subepithelial target cells can determine the outcome and contribution to mucosal disturbance, diarrhea and inflammation.

This Special Issue is open for papers on toxins from enteropathogens or pathobionts which have an impact on the intestine. We invite researchers with experimental or clinical approaches from related scientific fields such as gastroenterology, microbiology, biochemistry, physiology, epidemiology, food safety and zoonosis research and more to submit an original article or a review article to the Toxins Special Issue “Enterotoxins and Mucosal Pathomechanisms”.

Dr. Roland Bücker
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 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 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.


  • enterotoxin-producing microorganisms
  • intestinal epithelial perturbation
  • mucosal pathogenesis
  • tight junction dysregulation and epithelial permeability
  • intestinal inflammation and cytokine pathways
  • epithelial damage and genotoxic effects
  • intestinal lesions and epithelial cell death induction
  • action on cytoskeleton regulation and signaling
  • epithelial transporters and channels
  • receptor binding and cellular trafficking

Published Papers (1 paper)

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CDT of Clostridioides difficile Induces MLC-Dependent Intestinal Barrier Dysfunction in HT-29/B6 Epithelial Cell Monolayers
Toxins 2023, 15(1), 54; https://doi.org/10.3390/toxins15010054 - 07 Jan 2023
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Background: Clostridioides difficile binary toxin (CDT) defines the hypervirulence of strains in nosocomial antibiotic-induced colitis with the highest mortality. The objective of our study was to investigate the impact of CDT on the intestinal epithelial barrier and to enlighten the underlying molecular mechanisms. Methods: [...] Read more.
Background: Clostridioides difficile binary toxin (CDT) defines the hypervirulence of strains in nosocomial antibiotic-induced colitis with the highest mortality. The objective of our study was to investigate the impact of CDT on the intestinal epithelial barrier and to enlighten the underlying molecular mechanisms. Methods: Functional measurements of epithelial barrier function by macromolecular permeability and electrophysiology were performed in human intestinal HT-29/B6 cell monolayers. Molecular analysis of the spatial distribution of tight junction protein and cytoskeleton was performed by super-resolution STED microscopy. Results: Sublethal concentrations of CDT-induced barrier dysfunction with decreased TER and increased permeability for 332 Da fluorescein and 4 kDa FITC-dextran. The molecular correlate to the functional barrier defect by CDT was found to be a tight junction protein subcellular redistribution with tricellulin, occludin, and claudin-4 off the tight junction domain. This redistribution was shown to be MLCK-dependent. Conclusions: CDT compromised epithelial barrier function in a human intestinal colonic cell model, even in sublethal concentrations, pointing to barrier dysfunction in the intestine and leak flux induction as a diarrheal mechanism. However, this cannot be attributed to the appearance of apoptosis and necrosis, but rather to an opening of the paracellular leak pathway as the result of epithelial tight junction alterations. Full article
(This article belongs to the Special Issue Enterotoxins and Mucosal Pathomechanisms)
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