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Toxins
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Escherichia coli Toxins and Intestinal Diseases
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Escherichia coli Toxins and Intestinal Diseases

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

Deadline for manuscript submissions: closed (14 June 2021) | Viewed by 23992

Special Issue Editor

Dr. Roland Bücker

E-Mail Website
Guest Editor
Inst. Clinical Physiology / Nutritional Medicine, Dept. Gastroenterology, Charité – Universitätsmedizin Berlin, 10117 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
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Escherichia coli toxins comprise a variety of different pathologies in the gut. The pathomechanisms of endo- and exotoxins (ST and LT enterotoxins, Shiga-like toxins, etc.) from classical enteropathogenic E. coli pathovars (EPEC, ETEC, STEC, etc.) or in particular exotoxins from facultative pathogenic strains for the intestine (e.g., UPEC) are of high scientific interest for the understanding of different intestinal pathologies, including diarrhea, inflammatory bowel disease (IBD), or colorectal cancer.

There is still a gap of knowledge on the pathogenetic principles and pathomechanisms of different E. coli toxins in intestinal mucosal damage. Toxins secreted by pathobiont E. coli strains (e.g. HlyA, CNF, CDT, or colibactin) are associated with intestinal lesions, epithelial barrier dysfunction, polarity changes, inflammation, or metaplasia. RTX-type hemolysins (HlyA, etc.) are associated with lesions in IBD or colorectal cancer, and intestinal metastasis tissues have been shown to be colonized by E. coli expressing HlyA and colibactin. Furthermore, E. coli SPATEs show toxinogenic properties in intestinal host cells.

However, the general impact and burden of E. coli toxins in gastrointestinal pathophysiology is not yet sufficiently described. An understanding of E. coli toxin effects on receptor interaction, cell signaling pathways, immune cell–epithelial cell interaction, epithelial barrier function, or on subepithelial (immune or neuroendocrine) cells will facilitate future protective or therapeutic approaches.

The purpose of this Special Issue is thus to gather research on the E. coli toxin–host interactions and on the infection or colonization by toxin-producing E. coli with related intestinal diseases.

This Special Issue is open for works on toxins from all E. coli phylotypes or pathovars which have an impact on the intestine. We invite researchers with experimental or clinical approaches from all scientific fields (gastroenterology, microbiology, epidemiology, biochemistry, physiology, etc.) to submit an original article or review to Toxins.

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 2700 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

  • Toxin-producing Escherichia coli
  • Pathogenesis
  • Epidemiology
  • Epithelial damage
  • Intestinal epithelial permeability and tight junction regulation
  • Intestinal inflammation
  • Epithelial cell death induction and intestinal lesions
  • Cell dissemination
  • Epithelial-to-mesenchymal transition (EMT)
  • Colorectal cancer progression

Published Papers (6 papers)

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Research

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16 pages, 2318 KiB  
Article
Scalable Reporter Assays to Analyze the Regulation of stx2 Expression in Shiga Toxin-Producing Enteropathogens
by Martin B. Koeppel, Jana Glaser, Tobias Baumgartner, Stefanie Spriewald, Roman G. Gerlach, Benedikt von Armansperg, John M. Leong and Bärbel Stecher
Toxins 2021, 13(8), 534; https://0-doi-org.brum.beds.ac.uk/10.3390/toxins13080534 - 29 Jul 2021
Cited by 1 | Viewed by 2557
Abstract
Stx2 is the major virulence factor of EHEC and is associated with an increased risk for HUS in infected patients. The conditions influencing its expression in the intestinal tract are largely unknown. For optimal management and treatment of infected patients, the identification of [...] Read more.
Stx2 is the major virulence factor of EHEC and is associated with an increased risk for HUS in infected patients. The conditions influencing its expression in the intestinal tract are largely unknown. For optimal management and treatment of infected patients, the identification of environmental conditions modulating Stx2 levels in the human gut is of central importance. In this study, we established a set of chromosomal stx2 reporter assays. One system is based on superfolder GFP (sfGFP) using a T7 polymerase/T7 promoter-based amplification loop. This reporter can be used to analyze stx2 expression at the single-cell level using FACSs and fluorescence microscopy. The other system is based on the cytosolic release of the Gaussia princeps luciferase (gluc). This latter reporter proves to be a highly sensitive and scalable reporter assay that can be used to quantify reporter protein in the culture supernatant. We envision that this new set of reporter tools will be highly useful to comprehensively analyze the influence of environmental and host factors, including drugs, small metabolites and the microbiota, on Stx2 release and thereby serve the identification of risk factors and new therapies in Stx-mediated pathologies. Full article
(This article belongs to the Special Issue Escherichia coli Toxins and Intestinal Diseases)
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22 pages, 18849 KiB  
Article
Escherichia coli Alpha-Hemolysin HlyA Induces Host Cell Polarity Changes, Epithelial Barrier Dysfunction and Cell Detachment in Human Colon Carcinoma Caco-2 Cell Model via PTEN-Dependent Dysregulation of Cell Junctions
by Emanuel Schulz, Michael Schumann, Martina Schneemann, Violaine Dony, Anja Fromm, Oliver Nagel, Jörg-Dieter Schulzke and Roland Bücker
Toxins 2021, 13(8), 520; https://0-doi-org.brum.beds.ac.uk/10.3390/toxins13080520 - 26 Jul 2021
Cited by 8 | Viewed by 3383
Abstract
Escherichia coli (E. coli) of the B2 phylotype reside in human and animal intestines. The bacteria possess pathogenicity factors such as α-hemolysin (HlyA) that can induce intestinal epithelial leaks. We addressed the questions which host cell processes were dysregulated by E. [...] Read more.
Escherichia coli (E. coli) of the B2 phylotype reside in human and animal intestines. The bacteria possess pathogenicity factors such as α-hemolysin (HlyA) that can induce intestinal epithelial leaks. We addressed the questions which host cell processes were dysregulated by E. coli HlyA that can potentiate intestinal diseases. The colon carcinoma cell line Caco-2 was infected by HlyA+ E. coli. Cell polarity regulation was analyzed by live cell imaging for the phosphatidylinositol-4,5-bisphosphate (PIP2) abundance. In Caco-2 monolayers, transepithelial electrical resistance was measured for characterization of barrier function. Cell proliferation and separation were assessed microscopically. Epithelial regulation and cell signaling were analyzed by RNA-Seq and Ingenuity Pathway Analysis (IPA). Our main findings from E. coli HlyA toxinogenicity in the colon carcinoma cell line are that (i) PIP2 at the membrane decrease, (ii) PTEN (phosphatase and tensin homolog) inhibition leads to cell polarity changes, (iii) epithelial leakiness follows these polarity changes by disruption of cell junctions and (iv) epithelial cell detachment increases. HlyA affected pathways, e.g., the PTEN and metastasis signaling, were identified by RNA-Seq bioinformatics calculations in IPA. In conclusion, HlyA affects cell polarity, thereby inducing epithelial barrier dysfunction due to defective tight junctions and focal leak induction as an exemplary mechanism for leaky gut. Full article
(This article belongs to the Special Issue Escherichia coli Toxins and Intestinal Diseases)
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15 pages, 4657 KiB  
Article
Heat-Labile Toxin from Enterotoxigenic Escherichia coli Causes Systemic Impairment in Zebrafish Model
by Camila Henrique, Maria Alice Pimentel Falcão, Luciana De Araújo Pimenta, Adolfo Luís Almeida Maleski, Carla Lima, Thais Mitsunari, Sandra Coccuzzo Sampaio, Mônica Lopes-Ferreira and Roxane Maria Fontes Piazza
Toxins 2021, 13(6), 419; https://0-doi-org.brum.beds.ac.uk/10.3390/toxins13060419 - 12 Jun 2021
Cited by 2 | Viewed by 3148
Abstract
Heat-labile toxin I (LT-I), produced by strains of enterotoxigenic Escherichia coli (ETEC), causes profuse watery diarrhea in humans. Different in vitro and in vivo models have already elucidated the mechanism of action of this toxin; however, their use does not always allow for [...] Read more.
Heat-labile toxin I (LT-I), produced by strains of enterotoxigenic Escherichia coli (ETEC), causes profuse watery diarrhea in humans. Different in vitro and in vivo models have already elucidated the mechanism of action of this toxin; however, their use does not always allow for more specific studies on how the LT-I toxin acts in systemic tracts and intestinal cell lines. In the present work, zebrafish (Danio rerio) and human intestinal cells (Caco-2) were used as models to study the toxin LT-I. Caco-2 cells were used, in the 62nd passage, at different cell concentrations. LT-I was conjugated to FITC to visualize its transport in cells, as well as microinjected into the caudal vein of zebrafish larvae, in order to investigate its effects on survival, systemic traffic, and morphological formation. The internalization of LT-I was visualized in 3 × 104 Caco-2 cells, being associated with the cell membrane and nucleus. The systemic traffic of LT-I in zebrafish larvae showed its presence in the cardiac cavity, yolk, and regions of the intestine, as demonstrated by cardiac edema (100%), the absence of a swimming bladder (100%), and yolk edema (80%), in addition to growth limitation in the larvae, compared to the control group. There was a reduction in heart rate during the assessment of larval survival kinetics, demonstrating the cardiotoxic effect of LT-I. Thus, in this study, we provide essential new depictions of the features of LT-I. Full article
(This article belongs to the Special Issue Escherichia coli Toxins and Intestinal Diseases)
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Review

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15 pages, 1882 KiB  
Review
Shining a Light on Colibactin Biology
by Michael W. Dougherty and Christian Jobin
Toxins 2021, 13(5), 346; https://0-doi-org.brum.beds.ac.uk/10.3390/toxins13050346 - 12 May 2021
Cited by 33 | Viewed by 7253
Abstract
Colibactin is a secondary metabolite encoded by the pks gene island identified in several Enterobacteriaceae, including some pathogenic Escherichia coli (E. coli) commonly enriched in mucosal tissue collected from patients with inflammatory bowel disease and colorectal cancer. E. coli harboring this [...] Read more.
Colibactin is a secondary metabolite encoded by the pks gene island identified in several Enterobacteriaceae, including some pathogenic Escherichia coli (E. coli) commonly enriched in mucosal tissue collected from patients with inflammatory bowel disease and colorectal cancer. E. coli harboring this biosynthetic gene cluster cause DNA damage and tumorigenesis in cell lines and pre-clinical models, yet fundamental knowledge regarding colibactin function is lacking. To accurately assess the role of pks+ E. coli in cancer etiology, the biological mechanisms governing production and delivery of colibactin by these bacteria must be elucidated. In this review, we will focus on recent advances in our understanding of colibactin’s structural mode-of-action and mutagenic potential with consideration for how this activity may be regulated by physiologic conditions within the intestine. Full article
(This article belongs to the Special Issue Escherichia coli Toxins and Intestinal Diseases)
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12 pages, 1666 KiB  
Review
Impact of the Escherichia coli Heat-Stable Enterotoxin b (STb) on Gut Health and Function
by Shahnawaz Butt, Mazen Saleh and Jeffrey Gagnon
Toxins 2020, 12(12), 760; https://0-doi-org.brum.beds.ac.uk/10.3390/toxins12120760 - 02 Dec 2020
Cited by 7 | Viewed by 4486
Abstract
Enterotoxigenic Escherichia coli (ETEC) produces the heat-stable enterotoxin b (STb), which is responsible for secretory diarrhea in humans and animals. This toxin is secreted within the intestinal lumen of animals and humans following ETEC colonization, becoming active on enterocytes and altering fluid homeostasis. [...] Read more.
Enterotoxigenic Escherichia coli (ETEC) produces the heat-stable enterotoxin b (STb), which is responsible for secretory diarrhea in humans and animals. This toxin is secreted within the intestinal lumen of animals and humans following ETEC colonization, becoming active on enterocytes and altering fluid homeostasis. Several studies have outlined the nature of this toxin and its effects on gut health and the integrity of the intestinal epithelium. This review summarizes the mechanisms of how STb alters the gastrointestinal tract. These include the manipulation of mucosal tight junction protein integrity, the formation of enterocyte cellular pores and toxin internalization and the stimulation of programmed cell death. We conclude with insights into the potential link between STb intoxication and altered gut hormone regulation, and downstream physiology. Full article
(This article belongs to the Special Issue Escherichia coli Toxins and Intestinal Diseases)
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Other

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7 pages, 7172 KiB  
Brief Report
Switching Shiga Toxin (Stx) Type from Stx2d to Stx2a but Not Stx2c Alters Virulence of Stx-Producing Escherichia coli (STEC) Strain B2F1 in Streptomycin (Str)-Treated Mice
by Beth A. McNichol, Rebecca A. Bova, Kieron Torres, Lan N. Preston and Angela R. Melton-Celsa
Toxins 2021, 13(1), 64; https://0-doi-org.brum.beds.ac.uk/10.3390/toxins13010064 - 15 Jan 2021
Cited by 1 | Viewed by 1826
Abstract
Shiga toxin (Stx)-producing Escherichia coli (STEC) strain B2F1 produces Stx type 2d, a toxin that becomes more toxic towards Vero cells in the presence of intestinal mucus. STEC that make Stx2d are more pathogenic to streptomycin (Str)-treated mice than most STEC that produce [...] Read more.
Shiga toxin (Stx)-producing Escherichia coli (STEC) strain B2F1 produces Stx type 2d, a toxin that becomes more toxic towards Vero cells in the presence of intestinal mucus. STEC that make Stx2d are more pathogenic to streptomycin (Str)-treated mice than most STEC that produce Stx2a or Stx2c. However, purified Stx2d is only 2- or 7-fold more toxic by the intraperitoneal route than Stx2a or Stx2c, respectively. We hypothesized, therefore, that the toxicity differences among Stx2a, Stx2c, and Stx2d occur at the level of delivery from the intestine. To evaluate that hypothesis, we altered the toxin type produced by stx2d+ mouse virulent O91:H21 clinical isolate B2F1 to Stx2a or Stx2c. Because B2F1 encodes two copies of stx2d, we did these studies in a derivative of B2F1 in which stx2d1 was deleted. Although the strains were equivalently virulent to the Str-treated mice at the 1010 dose, the B2F1 strain that produced Stx2a was attenuated relative to the ones that produced Stx2d or Stx2c when administered at 103 CFU/mouse. We next compared the oral toxicities of purified Stx2a, Stx2c, and Stx2d. We found that purified Stx2d is more toxic than Stx2a or Stx2c upon oral administration at 4 µg/mouse. Taken together, these studies suggest that Stx2 toxins are most potent when delivered directly from the bacterium. Furthermore, because Stx2d and Stx2c have the identical amino acid composition in the toxin B subunit, our results indicate that the virulence difference between Stx2a and Stx2d and Stx2c resides in the B or binding subunit of the toxins. Full article
(This article belongs to the Special Issue Escherichia coli Toxins and Intestinal Diseases)
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