Special Issue "Enterotoxins: Microbial Proteins and Host Cell Dysregulation"
Deadline for manuscript submissions: 15 September 2014
Dr. Teresa Krakauer
Department of Immunology, Integrated Toxicology Division, United States Army Medical Research, Institute of Infectious Diseases, Fort Detrick, Frederick, MD 21702, USA
Phone: +1 301 619 4733
Fax: +1 301 619 2348
Enterotoxins encompass a diverse group of microbial toxins affecting the gut and are major contributors to bacterial food borne illness, gastrointestinal and systemic diseases for which limited therapeutics are available. Although the pathogenic effects arise from mucosal perturbation, dysregulation of immune cells through mediator release, cell activation or damage are major factors disrupting homeostasis in gut mucosa. Whereas proinflammatory cytokines and chemokines mediate toxic shock induced by staphylococcal enterotoxins, apoptosis and cytotoxic events are responsible for Clostridium perfringens enterotoxin and cholera toxin. Understanding of receptors, signaling pathways and the communication between cells of the gastrointestinal tract, immune and neuroendocrine system will facilitate the development of new therapeutics.
Dr. Teresa Krakauer
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).
- receptor and signaling mechanism
- mucosal perturbation
- targeted therapeutics
Review: Update on Staphylococcal Superantigen-Induced Signaling Pathways and Therapeutic Interventions
Toxins 2013, 5(9), 1629-1654; doi:10.3390/toxins5091629
Received: 8 July 2013; in revised form: 13 September 2013 / Accepted: 13 September 2013 / Published: 24 September 2013| Download PDF Full-text (476 KB) | View HTML Full-text | Download XML Full-text
Article: Treatment with the Hyaluronic Acid Synthesis Inhibitor 4-Methylumbelliferone Suppresses SEB-Induced Lung Inflammation
Toxins 2013, 5(10), 1814-1826; doi:10.3390/toxins5101814
Received: 14 August 2013; in revised form: 3 October 2013 / Accepted: 12 October 2013 / Published: 17 October 2013| Download PDF Full-text (1357 KB) | View HTML Full-text | Download XML Full-text
Toxins 2013, 5(10), 1859-1871; doi:10.3390/toxins5101859
Received: 8 August 2013; in revised form: 9 October 2013 / Accepted: 10 October 2013 / Published: 22 October 2013| Download PDF Full-text (387 KB) | View HTML Full-text | Download XML Full-text
Toxins 2013, 5(11), 2138-2160; doi:10.3390/toxins5112138
Received: 1 October 2013; in revised form: 30 October 2013 / Accepted: 31 October 2013 / Published: 12 November 2013| Download PDF Full-text (334 KB) | View HTML Full-text | Download XML Full-text
Review: Soluble T Cell Receptor Vβ Domains Engineered for High-Affinity Binding to Staphylococcal or Streptococcal Superantigens
Toxins 2014, 6(2), 556-574; doi:10.3390/toxins6020556
Received: 16 December 2013; in revised form: 21 January 2014 / Accepted: 22 January 2014 / Published: 28 January 2014| Download PDF Full-text (761 KB)
The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.
Type of Paper: Review
Title: Clostridium perfringens Epsilon Toxin
Authors: Bradley G. Stiles 1, Holger Barth 2 and Michel R. Popoff 3
Affiliations: 1 Biology Department, Wilson College, Chambersburg, Pennsylvania, USA; E-Mail: firstname.lastname@example.org
2 Institute of Pharmacology and Toxicology, University of Ulm Medical Center, Ulm, Germany; E-Mail: email@example.com
3 Institut Pasteur, Bactéries anaérobies et Toxines, 25 rue du Dr Roux, 75724 Paris Cedex 15, France; E-Mail: firstname.lastname@example.org
Abstract: Epsilon toxin is a 33 kDa protein produced by Clostridium perfringens (types B and D) and involved in fatal cattle, goat, as well as sheep enteric disease. Epsilon toxin belongs to the aerolysin-toxin family (Aeromonas hydrophila aerolysin and Clostridium septicum alpha toxin), contains three distinct domains, is proteolytically-activated, and forms oligomeric pores on cell surfaces. Vaccination is available to control disease, but therapeutic measures are currently lacking. An overview of epsilon toxin biochemistry, disease characteristics in various animals, and control mechanisms will be shared with the reader.
Type of Paper: Article
Title: Treatment with the Hyaluronic Acid Synthesis Inhibitor 4-Methylumbelliferone Suppresses SEB-Induced Lung Inflammation
Authors: Robert J. McKallip *, Harriet Hagele and Olga N. Uchakina
Affiliation: Division of Basic Medical Sciences, Mercer University School of Medicine, 1550 College Street, Macon, GA 31207, USA
* Author to whom correspondence should be addressed; E-Mail: email@example.com; Tel.: +1-478-301-2779+1-478-301-2779; Fax: +1-478-301-5487.
Abstract: Exposure to bacterial superantigens, such as staphylococcal enterotoxin B (SEB), can lead to the induction of acute lung injury/acute respiratory distress syndrome (ALI/ARDS). To date, there are no known effective treatments for SEB-induced inflammation. In the current study we investigated the potential use of the hyaluronic acid synthase inhibitor 4-methylumbelliferone (4-MU) on staphylococcal enterotoxin B (SEB) induced acute lung inflammation. Culturing SEB-activated immune cells with 4-MU led to reduced proliferation, reduced cytokine production as well as an increase in apoptosis when compared to untreated cells. Treatment of mice with 4-MU led to reduced HA production and to protection of mice from SEB-induced lung injury. Specifically, 4-MU treatment led to a reduction in SEB-induced lung permeability, and reduced pro-inflammatory cytokine production. Taken together, these results suggest that use of 4-MU to target hyaluronic acid production may be an effective treatment for the inflammatory response following exposure to SEB.
Type of Paper: Review
Title: Redox Regulation of Toxinogenesis by Bacillus cereus
Authors: Catherine Duport 1,2,* and Thierry Clavel 1,2
Affiliations: 1 Université d’Avignon et des Pays de Vaucluse, UMR408, Sécurité et Qualité des Produits d’Origine Végétale, F-84000 Avignon, France
2 INRA, UMR408, Sécurité et Qualité des Produits d’Origine végétale, F-84914 Avignon, France
* Author to whom correspondence should be addressed; E-Mail: firstname.lastname@example.org
Abstract: Redox reactions are central to both catabolic and anabolic metabolism. The ability to maintain redox balance is thus vital to all pathogens. Various regulatory sensors continually monitor the redox state of the internal and external environments and control the pathways that regulate redox homeostasis. This review focuses on how key redox-dependent transcription factors and signal-transduction pathways control both catabolism and enterotoxin synthesis in Bacillus cereus. The current understanding of how disturbance in redox homeostasis may affect toxinogenesis and contribute to the development of pathogenesis is reviewed. We also discuss how the knowledge on redox regulation of catabolism can be used to predict the diarrheal potential of a B. cereus strain, which is essentially dictated by the amount of secreted nonhemolytic enterotoxin Nhe.
Last update: 4 March 2014