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Toxins
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Cytotoxic Necrotizing Factors
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Cytotoxic Necrotizing Factors

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

Deadline for manuscript submissions: closed (31 October 2013) | Viewed by 20849

Special Issue Editor

Dr. Alessia Fabbri

E-Mail Website
Guest Editor
Department of Cardiovascular, Endocrine-Metabolic Diseases and Aging, Istituto Superiore di Sanità, 00161 Rome, Italy
Interests: bacterial protein toxins; Rho GTPases; actin cytoskeleton; mitochondria; cellular microbiology; cancer; toxins as therapeutics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The cytotoxic necrotising factor (CNF) family of proteins includes bacterial cytotoxic necrotizing factors proteins from Escherichia coli and the related dermonecrotic toxin from Bordetella species. Very recently, also Yersinia pseudotubercolosis have been reported to produce a CNF. These toxins are single chain polypeptides consisting of an N-terminal domain responsible for binding to target cells and a C-terminal domain responsible for the catalytic activity. CNFs and DNT act on the small GTPases of the Rho family through deamidation and/or transglutamination of a Gln residue of the active site, which results in activation of the G proteins and their cognate downstream signaling pathways. In particular, CNFs deamidate Gln63 of Rho or the corresponding Gln61 of Rac and Cdc42 whereas DNT deamidates or polyaminates the Glns with ubiquitous polyamines such as spermine, putresceine and spermidine.

The mechanism of action of CNFs and DNT is now well defined. However, several questions remain as to secretion from bacteria, receptors and translocation into the cytosol.

This special issue aims to provide the state of the art in the research on CNFs and, thus, it will deal with major achievements and recent discoveries on CNFs including three-dimensional structures, activities, toxin receptors, toxin trafficking and clinical applications.

Prof. Dr. Alessia Fabbri
Guest Editor

Submission

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. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as 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 refereed through a 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 1000 CHF (Swiss Francs).

Keywords

  • Exotoxin
  • virulence factor
  • Rho GTPase
  • Escherichia coli
  • Bordetella sp.
  • Yersinia pseudotubercolosis

Published Papers (3 papers)

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Research

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1168 KiB  
Article
The E. coli CNF1 as a Pioneering Therapy for the Central Nervous System Diseases
by Sara Travaglione, Stefano Loizzo, Giulia Ballan, Carla Fiorentini and Alessia Fabbri
Toxins 2014, 6(1), 270-282; https://doi.org/10.3390/toxins6010270 - 07 Jan 2014
Cited by 10 | Viewed by 6678
Abstract
The Cytotoxic Necrotizing Factor 1 (CNF1), a protein toxin from pathogenic E. coli, modulates the Rho GTPases, thus, directing the organization of the actin cytoskeleton. In the nervous system, the Rho GTPases play a key role in several processes, controlling the morphogenesis [...] Read more.
The Cytotoxic Necrotizing Factor 1 (CNF1), a protein toxin from pathogenic E. coli, modulates the Rho GTPases, thus, directing the organization of the actin cytoskeleton. In the nervous system, the Rho GTPases play a key role in several processes, controlling the morphogenesis of dendritic spines and synaptic plasticity in brain tissues. This review is focused on the peculiar property of CNF1 to enhance brain plasticity in in vivo animal models of central nervous system (CNS) diseases, and on its possible application in therapy. Full article
(This article belongs to the Special Issue Cytotoxic Necrotizing Factors)
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1447 KiB  
Article
Activation of RhoA,B,C by Yersinia Cytotoxic Necrotizing Factor (CNFy) Induces Apoptosis in LNCaP Prostate Cancer Cells
by Anke Augspach, Joachim H. List, Philipp Wolf, Heike Bielek, Carsten Schwan, Ursula Elsässer-Beile, Klaus Aktories and Gudula Schmidt
Toxins 2013, 5(11), 2241-2257; https://doi.org/10.3390/toxins5112241 - 21 Nov 2013
Cited by 15 | Viewed by 7578
Abstract
Prostate cancer is the most common malignancy, accounting for about 25% of all incident cases among men in industrialized countries. The human androgen-dependent prostate cancer cell line LNCaP, which is derived from a metastatic lesion of human prostatic adenocarcinoma, is frequently used to [...] Read more.
Prostate cancer is the most common malignancy, accounting for about 25% of all incident cases among men in industrialized countries. The human androgen-dependent prostate cancer cell line LNCaP, which is derived from a metastatic lesion of human prostatic adenocarcinoma, is frequently used to study prostate cancer associated signaling pathways in vitro. Recently it was described that Rho GTPase activation in these cells leads to apoptotic responses. We used the bacterial toxins CNFy and CNF1, which specifically and directly activate Rho GTPases by deamidation of a single glutamine. We asked whether these Rho activators could induce apoptosis in LNCaP cells. Our results indicate that RhoA activation, induced by CNFy, does lead to intrinsic apoptosis of the cells. Analysis of the underlying signaling pathway reveals that apoptosis induction requires the activity of Rho kinase (ROCK) and myosin activation, an apoptotic pathway previously identified in cancer stem cells. Full article
(This article belongs to the Special Issue Cytotoxic Necrotizing Factors)
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Review

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Review
Cytotoxic Necrotizing Factor 1 Contributes to Escherichia coli Meningitis
by Ming-Hsien Wang and Kwang Sik Kim
Toxins 2013, 5(11), 2270-2280; https://doi.org/10.3390/toxins5112270 - 22 Nov 2013
Cited by 23 | Viewed by 5696
Abstract
E. coli is the most common Gram-negative bacteria causing neonatal meningitis, and E. coli meningitis continues to be an important cause of mortality and morbidity throughout the world. Recent reports of E. coli meningitis caused by antimicrobial resistant strains are a particular concern. [...] Read more.
E. coli is the most common Gram-negative bacteria causing neonatal meningitis, and E. coli meningitis continues to be an important cause of mortality and morbidity throughout the world. Recent reports of E. coli meningitis caused by antimicrobial resistant strains are a particular concern. These findings indicate that a novel strategy is needed to identify new targets for prevention and therapy of E. coli meningitis. Cytotoxic necrotizing factor 1 (CNF1) is a bacterial virulence factor associated principally with E. coli strains causing urinary tract infection and meningitis. We have shown that CNF1 contributes to E. coli invasion of the blood-brain barrier and penetration into the brain, the essential step in the development of E. coli meningitis, and identified the host receptor for CNF1, 37-kDa laminin receptor precursor (37LRP). CNF1, however, is a cytoplasmic protein and its contribution to E. coli invasion of the blood-brain barrier requires its secretion from the bacterial cytoplasm. No signal peptide is found in the CNF1 sequence. CNF1 secretion is, therefore, a strategy utilized by meningitis-causing E. coli to invade the blood-brain barrier. Elucidation of the mechanisms involved in CNF1 secretion, as shown in this report with the involvement of Fdx and YgfZ provides the novel information on potential targets for prevention and therapy of E. coli meningitis by virtue of targeting the secretion of CNF1. Full article
(This article belongs to the Special Issue Cytotoxic Necrotizing Factors)
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