Special Issue "Pathogenesis of Hemolytic Uremic Syndrome Caused by Shiga Toxin-Producing Escherichia coli Infections"

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

Deadline for manuscript submissions: 30 November 2019.

Special Issue Editor

Prof. Maurizio Brigotti
E-Mail Website
Guest Editor
Dipartimento di Medicina Specialistica, Diagnostica e Sperimentale (DIMES), Sede di Patologia Generale, Università di Bologna, Via San Giacomo, 14, 40126 Bologna, Italy

Special Issue Information

Dear Colleagues,

Human infections by Shiga toxin-producing Escherichia coli (STEC) cause severe and life-threatening diseases. These powerful pathogens are capable of elaborating a wide array of virulence factors which often overwhelm the host defense system. In particular, the exotoxins produced by these pathogenic E. coli strains, namely Shiga toxins, are the key bacterial factors responsible for hemolytic uremic syndrome (HUS), the main cause of acute renal failure in early childhood.

The pathogenesis of HUS is puzzling and not completely understood, despite a great deal of investigation. Toxins target host endothelial cells in the kidney and brain during the ultimate toxemic phase, culminating in HUS. However, a plethora of complex, concurrent and interactive phenomena occur during precocious toxemia when Shiga toxins interact with numerous blood components (neutrophils, monocytes, platelets, erythrocytes, human serum amyloid protein, complement factor H, and Toll-like receptor 4). The formation of platelet–leukocyte aggregates, the release of extracellular vesicles containing HUS-triggering pathogenic factors and the activation of complement system are well known consequences.

This Special Issue is aimed at focusing on all aspects of the interaction of Shiga toxins with host cell and/or molecules involved in the pathogenesis of STEC-induced HUS. The various papers dealing with specific arguments are expected to bring renewed insight on focalized topics, fostering our understanding of the general picture, as well as the single details of a canvas unveil their message only when they are considered in the general context.

Prof. Maurizio Brigotti
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 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.


  • Hemolytic uremic syndrome
  • pathogenesis
  • pathogen-host interactions
  • Shiga toxins
  • Shiga toxin-producing Escherichia coli
  • STEC infections

Published Papers (1 paper)

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Open AccessArticle
Crosstalk between Human Microvascular Endothelial Cells and Tubular Epithelial Cells Modulates Pro-Inflammatory Responses Induced by Shiga Toxin Type 2 and Subtilase Cytotoxin
Toxins 2019, 11(11), 648; https://doi.org/10.3390/toxins11110648 - 07 Nov 2019
Hemolytic uremic syndrome (HUS) is a consequence of Shiga toxin (Stx)-producing Escherichia coli (STEC) infection and is the most frequent cause of acute renal failure (ARF) in children. Subtilase cytotoxin (SubAB) has also been associated with HUS pathogenesis. We previously reported that Stx2 [...] Read more.
Hemolytic uremic syndrome (HUS) is a consequence of Shiga toxin (Stx)-producing Escherichia coli (STEC) infection and is the most frequent cause of acute renal failure (ARF) in children. Subtilase cytotoxin (SubAB) has also been associated with HUS pathogenesis. We previously reported that Stx2 and SubAB cause different effects on co-cultures of human renal microvascular endothelial cells (HGEC) and human proximal tubular epithelial cells (HK-2) relative to HGEC and HK-2 monocultures. In this work we have analyzed the secretion of pro-inflammatory cytokines by co-cultures compared to monocultures exposed or not to Stx2, SubAB, and Stx2+SubAB. Under basal conditions, IL-6, IL-8 and TNF-α secretion was different between monocultures and co-cultures. After toxin treatments, high concentrations of Stx2 and SubAB decreased cytokine secretion by HGEC monocultures, but in contrast, low toxin concentrations increased their release. Toxins did not modulate the cytokine secretion by HK-2 monocultures, but increased their release in the HK-2 co-culture compartment. In addition, HK-2 monocultures were stimulated to release IL-8 after incubation with HGEC conditioned media. Finally, Stx2 and SubAB were detected in HGEC and HK-2 cells from the co-cultures. This work describes, for the first time, the inflammatory responses induced by Stx2 and SubAB, in a crosstalk model of renal endothelial and epithelial cells. Full article
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