Staphylococcus Aureus Superantigen-Like Protein SSL1: a Toxic Protease
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The Role of Streptococcal and Staphylococcal Exotoxins and Proteases in Human Necrotizing Soft Tissue Infections
toxins Review The Role of Streptococcal and Staphylococcal Exotoxins and Proteases in Human Necrotizing Soft Tissue Infections Patience Shumba 1, Srikanth Mairpady Shambat 2 and Nikolai Siemens 1,* 1 Center for Functional Genomics of Microbes, Department of Molecular Genetics and Infection Biology, University of Greifswald, D-17489 Greifswald, Germany; [email protected] 2 Division of Infectious Diseases and Hospital Epidemiology, University Hospital Zurich, University of Zurich, CH-8091 Zurich, Switzerland; [email protected] * Correspondence: [email protected]; Tel.: +49-3834-420-5711 Received: 20 May 2019; Accepted: 10 June 2019; Published: 11 June 2019 Abstract: Necrotizing soft tissue infections (NSTIs) are critical clinical conditions characterized by extensive necrosis of any layer of the soft tissue and systemic toxicity. Group A streptococci (GAS) and Staphylococcus aureus are two major pathogens associated with monomicrobial NSTIs. In the tissue environment, both Gram-positive bacteria secrete a variety of molecules, including pore-forming exotoxins, superantigens, and proteases with cytolytic and immunomodulatory functions. The present review summarizes the current knowledge about streptococcal and staphylococcal toxins in NSTIs with a special focus on their contribution to disease progression, tissue pathology, and immune evasion strategies. Keywords: Streptococcus pyogenes; group A streptococcus; Staphylococcus aureus; skin infections; necrotizing soft tissue infections; pore-forming toxins; superantigens; immunomodulatory proteases; immune responses Key Contribution: Group A streptococcal and Staphylococcus aureus toxins manipulate host physiological and immunological responses to promote disease severity and progression. 1. Introduction Necrotizing soft tissue infections (NSTIs) are rare and represent a more severe rapidly progressing form of soft tissue infections that account for significant morbidity and mortality [1]. -
Corynebacterium Diphtheriae Strains Correlates with the Predicted Membrane- Associated and Secreted Proteome Vartul Sangal1*, Jochen Blom2, Iain C
Sangal et al. BMC Genomics (2015) 16:765 DOI 10.1186/s12864-015-1980-8 RESEARCH ARTICLE Open Access Adherence and invasive properties of Corynebacterium diphtheriae strains correlates with the predicted membrane- associated and secreted proteome Vartul Sangal1*, Jochen Blom2, Iain C. Sutcliffe1, Christina von Hunolstein3, Andreas Burkovski4 and Paul A. Hoskisson5 Abstract Background: Non-toxigenic Corynebacterium diphtheriae strains are emerging as a major cause of severe pharyngitis and tonsillitis as well as invasive diseases such as endocarditis, septic arthritis, splenic abscesses and osteomyelitis. C. diphtheriae strains have been reported to vary in their ability to adhere and invade different cell lines. To identify the genetic basis of variation in the degrees of pathogenicity, we sequenced the genomes of four strains of C. diphtheriae (ISS 3319, ISS 4060, ISS 4746 and ISS 4749) that are well characterised in terms of their ability to adhere and invade mammalian cells. Results: Comparative analyses of 20 C. diphtheriae genome sequences, including 16 publicly available genomes, revealed a pan-genome comprising 3,989 protein coding sequences that include 1,625 core genes and 2,364 accessory genes. Most of the genomic variation between these strains relates to uncharacterised genes encoding hypothetical proteins or transposases. Further analyses of protein sequences using an array of bioinformatic tools predicted most of the accessory proteome to be located in the cytoplasm. The membrane-associated and secreted proteins are generally involved in adhesion and virulence characteristics. The genes encoding membrane-associated proteins, especially the number and organisation of the pilus gene clusters (spa) including the number of genes encoding surface proteins with LPXTG motifs differed between different strains. -
Biological Toxins As the Potential Tools for Bioterrorism
International Journal of Molecular Sciences Review Biological Toxins as the Potential Tools for Bioterrorism Edyta Janik 1, Michal Ceremuga 2, Joanna Saluk-Bijak 1 and Michal Bijak 1,* 1 Department of General Biochemistry, Faculty of Biology and Environmental Protection, University of Lodz, Pomorska 141/143, 90-236 Lodz, Poland; [email protected] (E.J.); [email protected] (J.S.-B.) 2 CBRN Reconnaissance and Decontamination Department, Military Institute of Chemistry and Radiometry, Antoniego Chrusciela “Montera” 105, 00-910 Warsaw, Poland; [email protected] * Correspondence: [email protected] or [email protected]; Tel.: +48-(0)426354336 Received: 3 February 2019; Accepted: 3 March 2019; Published: 8 March 2019 Abstract: Biological toxins are a heterogeneous group produced by living organisms. One dictionary defines them as “Chemicals produced by living organisms that have toxic properties for another organism”. Toxins are very attractive to terrorists for use in acts of bioterrorism. The first reason is that many biological toxins can be obtained very easily. Simple bacterial culturing systems and extraction equipment dedicated to plant toxins are cheap and easily available, and can even be constructed at home. Many toxins affect the nervous systems of mammals by interfering with the transmission of nerve impulses, which gives them their high potential in bioterrorist attacks. Others are responsible for blockage of main cellular metabolism, causing cellular death. Moreover, most toxins act very quickly and are lethal in low doses (LD50 < 25 mg/kg), which are very often lower than chemical warfare agents. For these reasons we decided to prepare this review paper which main aim is to present the high potential of biological toxins as factors of bioterrorism describing the general characteristics, mechanisms of action and treatment of most potent biological toxins. -
Medical Management of Biologic Casualties Handbook
USAMRIID’s MEDICAL MANAGEMENT OF BIOLOGICAL CASUALTIES HANDBOOK Fourth Edition February 2001 U.S. ARMY MEDICAL RESEARCH INSTITUTE OF INFECTIOUS DISEASES ¨ FORT DETRICK FREDERICK, MARYLAND 1 Sources of information: National Response Center 1-800-424-8802 or (for chem/bio hazards & terrorist events) 1-202-267-2675 National Domestic Preparedness Office: 1-202-324-9025 (for civilian use) Domestic Preparedness Chem/Bio Help line: 1-410-436-4484 or (Edgewood Ops Center - for military use) DSN 584-4484 USAMRIID Emergency Response Line: 1-888-872-7443 CDC'S Bioterrorism Preparedness and Response Center: 1-770-488-7100 John's Hopkins Center for Civilian Biodefense: 1-410-223-1667 (Civilian Biodefense Studies) An Adobe Acrobat Reader (pdf file) version and a Palm OS Electronic version of this Handbook can both be downloaded from the Internet at: http://www.usamriid.army.mil/education/bluebook.html 2 USAMRIID’s MEDICAL MANAGEMENT OF BIOLOGICAL CASUALTIES HANDBOOK Fourth Edition February 2001 Editors: LTC Mark Kortepeter LTC George Christopher COL Ted Cieslak CDR Randall Culpepper CDR Robert Darling MAJ Julie Pavlin LTC John Rowe COL Kelly McKee, Jr. COL Edward Eitzen, Jr. Comments and suggestions are appreciated and should be addressed to: Operational Medicine Department Attn: MCMR-UIM-O U.S. Army Medical Research Institute of Infectious Diseases (USAMRIID) Fort Detrick, Maryland 21702-5011 3 PREFACE TO THE FOURTH EDITION The Medical Management of Biological Casualties Handbook, which has become affectionately known as the "Blue Book," has been enormously successful - far beyond our expectations. Since the first edition in 1993, the awareness of biological weapons in the United States has increased dramatically. -
SARS-Cov-2 As a Superantigen in Multisystem Inflammatory Syndrome in Children (MIS-C)
SARS-CoV-2 as a superantigen in multisystem inflammatory syndrome in children (MIS-C) Theodore Kouo, Worarat Chaisawangwong J Clin Invest. 2021. https://doi.org/10.1172/JCI149327. Commentary In-Press Preview Multisystem Inflammatory Syndrome in Children (MIS-C) is a rare but deadly new disease in children that rapidly progresses to hyperinflammation, shock, and can lead to multiple organ failure if unrecognized. It has been found to be temporally associated with the COVID-19 pandemic and is often associated with SARS-CoV-2 exposure in children. In this issue of the JCI, Porritt, Paschold, and Rivas et al. identify restricted T cell receptor (TCR) β-chain variable domain (Vβ) usage in patients with severe MIS-C indicating a potential role for SARS-CoV-2 as a superantigen. These findings suggest that a blood test that determines the presence of specific TCR beta variable gene segments (TRBV) may identify patients at risk for severe MIS-C. Find the latest version: https://jci.me/149327/pdf SARS-CoV-2 as a superantigen in multisystem inflammatory syndrome in children (MIS-C) Theodore Kouo1 and Worarat Chaisawangwong2 1Department of Pediatrics, Division of Emergency Medicine, 2Department of Pathology, Johns Hopkins University, School of Medicine, Baltimore, MD, USA. Address correspondence to: Theodore Kouo Johns Hopkins Children’s Center 1800 Orleans Street, G1509 Phone: 410-955-6146 Email: [email protected] COI Statement: The authors declare that no conflict of interest exists. Abstract Multisystem Inflammatory Syndrome in Children (MIS-C) is a rare but deadly new disease in children that rapidly progresses to hyperinflammation, shock, and can lead to multiple organ failure if unrecognized. -
Medical Management of Biological Casualties Handbook
USAMRIID’s MEDICAL MANAGEMENT OF BIOLOGICAL CASUALTIES HANDBOOK Sixth Edition April 2005 U.S. ARMY MEDICAL RESEARCH INSTITUTE OF INFECTIOUS DISEASES FORT DETRICK FREDERICK, MARYLAND Emergency Response Numbers National Response Center: 1-800-424-8802 or (for chem/bio hazards & terrorist events) 1-202-267-2675 National Domestic Preparedness Office: 1-202-324-9025 (for civilian use) Domestic Preparedness Chem/Bio Helpline: 1-410-436-4484 or (Edgewood Ops Center – for military use) DSN 584-4484 USAMRIID’s Emergency Response Line: 1-888-872-7443 CDC'S Emergency Response Line: 1-770-488-7100 Handbook Download Site An Adobe Acrobat Reader (pdf file) version of this handbook can be downloaded from the internet at the following url: http://www.usamriid.army.mil USAMRIID’s MEDICAL MANAGEMENT OF BIOLOGICAL CASUALTIES HANDBOOK Sixth Edition April 2005 Lead Editor Lt Col Jon B. Woods, MC, USAF Contributing Editors CAPT Robert G. Darling, MC, USN LTC Zygmunt F. Dembek, MS, USAR Lt Col Bridget K. Carr, MSC, USAF COL Ted J. Cieslak, MC, USA LCDR James V. Lawler, MC, USN MAJ Anthony C. Littrell, MC, USA LTC Mark G. Kortepeter, MC, USA LTC Nelson W. Rebert, MS, USA LTC Scott A. Stanek, MC, USA COL James W. Martin, MC, USA Comments and suggestions are appreciated and should be addressed to: Operational Medicine Department Attn: MCMR-UIM-O U.S. Army Medical Research Institute of Infectious Diseases (USAMRIID) Fort Detrick, Maryland 21702-5011 PREFACE TO THE SIXTH EDITION The Medical Management of Biological Casualties Handbook, which has become affectionately known as the "Blue Book," has been enormously successful - far beyond our expectations. -
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European Review for Medical and Pharmacological Sciences 2021; 25: 1622-1630 Superantigens, superantigen-like proteins and superantigen derivatives for cancer treatment J.-Y. CHEN Xiehe Biology Group, Nobel Institute of Medicine, Shenzhen, Guangdong Province, China Abstract. – OBJECTIVE: Bacterial superanti- gesting a more complex mechanism of immune gens (SAgs) are proteins produced by few types response6. Indeed, the current view is that SAgs of bacteria that have been linked to several hu- bind to multiple coreceptors forming a costimu- man diseases. Due to their potent in vitro and in latory axis between coreceptors critical for T-cell vivo tumoricidal effects, they are extensively in- 7 vestigated for oncological applications either activation . CD28 is a homodimer expressed alone or in combination with classical antican- constitutively on T cells that interacts with its cer drugs. However, the intrinsic toxicity of nat- B7 coligands expressed on antigen-presenting ural SAgs stimulated the development of more cells, transducing the signal essential for T cell effective and less toxic SAg-based immunother- activation. The staphylococcal superantigen-like apy. This review summarizes our current knowl- protein 1 (SSL1) specifically binds to human edge on SAg-based immunotherapy including extracellular signal-regulated kinase 2 (hERK2), SAg-like proteins and SAg derivatives, as well as their potential alone or with other therapeu- an important stress-activated kinase in mito- 8 tic modalities including chemotherapy and ra- gen-activated protein kinase signaling pathways . diotherapy. It is now clearer that SAgs induce the release of cytokines and chemokines through multiple Key Words: pathways as it was recently observed in in vitro Superantigen, Superantigen derivative, Superanti- 9 gen-like, Cancer, Combination therapy experiments . -
Report from the 26Th Meeting on Toxinology,“Bioengineering Of
toxins Meeting Report Report from the 26th Meeting on Toxinology, “Bioengineering of Toxins”, Organized by the French Society of Toxinology (SFET) and Held in Paris, France, 4–5 December 2019 Pascale Marchot 1,* , Sylvie Diochot 2, Michel R. Popoff 3 and Evelyne Benoit 4 1 Laboratoire ‘Architecture et Fonction des Macromolécules Biologiques’, CNRS/Aix-Marseille Université, Faculté des Sciences-Campus Luminy, 13288 Marseille CEDEX 09, France 2 Institut de Pharmacologie Moléculaire et Cellulaire, Université Côte d’Azur, CNRS, Sophia Antipolis, 06550 Valbonne, France; [email protected] 3 Bacterial Toxins, Institut Pasteur, 75015 Paris, France; michel-robert.popoff@pasteur.fr 4 Service d’Ingénierie Moléculaire des Protéines (SIMOPRO), CEA de Saclay, Université Paris-Saclay, 91191 Gif-sur-Yvette, France; [email protected] * Correspondence: [email protected]; Tel.: +33-4-9182-5579 Received: 18 December 2019; Accepted: 27 December 2019; Published: 3 January 2020 1. Preface This 26th edition of the annual Meeting on Toxinology (RT26) of the SFET (http://sfet.asso.fr/ international) was held at the Institut Pasteur of Paris on 4–5 December 2019. The central theme selected for this meeting, “Bioengineering of Toxins”, gave rise to two thematic sessions: one on animal and plant toxins (one of our “core” themes), and a second one on bacterial toxins in honour of Dr. Michel R. Popoff (Institut Pasteur, Paris, France), both sessions being aimed at emphasizing the latest findings on their respective topics. Nine speakers from eight countries (Belgium, Denmark, France, Germany, Russia, Singapore, the United Kingdom, and the United States of America) were invited as international experts to present their work, and other researchers and students presented theirs through 23 shorter lectures and 27 posters. -
Penetration of Stratified Mucosa Cytolysins Augment Superantigen
Cytolysins Augment Superantigen Penetration of Stratified Mucosa Amanda J. Brosnahan, Mary J. Mantz, Christopher A. Squier, Marnie L. Peterson and Patrick M. Schlievert This information is current as of September 25, 2021. J Immunol 2009; 182:2364-2373; ; doi: 10.4049/jimmunol.0803283 http://www.jimmunol.org/content/182/4/2364 Downloaded from References This article cites 76 articles, 24 of which you can access for free at: http://www.jimmunol.org/content/182/4/2364.full#ref-list-1 Why The JI? Submit online. http://www.jimmunol.org/ • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average by guest on September 25, 2021 Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2009 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Cytolysins Augment Superantigen Penetration of Stratified Mucosa1 Amanda J. Brosnahan,* Mary J. Mantz,† Christopher A. Squier,† Marnie L. Peterson,‡ and Patrick M. Schlievert2* Staphylococcus aureus and Streptococcus pyogenes colonize mucosal surfaces of the human body to cause disease. A group of virulence factors known as superantigens are produced by both of these organisms that allows them to cause serious diseases from the vaginal (staphylococci) or oral mucosa (streptococci) of the body. -
Nasopharyngeal Infection by Streptococcus Pyogenes Requires Superantigen-Responsive Vβ-Specific T Cells
Nasopharyngeal infection by Streptococcus pyogenes requires superantigen-responsive Vβ-specific T cells Joseph J. Zeppaa, Katherine J. Kaspera, Ivor Mohorovica, Delfina M. Mazzucaa, S. M. Mansour Haeryfara,b,c,d, and John K. McCormicka,c,d,1 aDepartment of Microbiology and Immunology, Schulich School of Medicine & Dentistry, Western University, London, ON N6A 5C1, Canada; bDepartment of Medicine, Division of Clinical Immunology & Allergy, Schulich School of Medicine & Dentistry, Western University, London, ON N6A 5A5, Canada; cCentre for Human Immunology, Western University, London, ON N6A 5C1, Canada; and dLawson Health Research Institute, London, ON N6C 2R5, Canada Edited by Philippa Marrack, Howard Hughes Medical Institute, National Jewish Health, Denver, CO, and approved July 14, 2017 (received for review January 18, 2017) The globally prominent pathogen Streptococcus pyogenes secretes context of invasive streptococcal disease is extremely dangerous, potent immunomodulatory proteins known as superantigens with a mortality rate of over 30% (10). (SAgs), which engage lateral surfaces of major histocompatibility The role of SAgs in severe human infections has been well class II molecules and T-cell receptor (TCR) β-chain variable domains established (5, 11, 12), and specific MHC-II haplotypes are known (Vβs). These interactions result in the activation of numerous Vβ- risk factors for the development of invasive streptococcal disease specific T cells, which is the defining activity of a SAg. Although (13), an outcome that has been directly linked to SAgs (14, 15). streptococcal SAgs are known virulence factors in scarlet fever However, how these exotoxins contribute to superficial disease and and toxic shock syndrome, mechanisms by how SAgs contribute colonization is less clear. -
Hemolysin CB with Human C5a Receptors Γ Valentine Leukocidin
Differential Interaction of the Staphylococcal Toxins Panton−Valentine Leukocidin and γ -Hemolysin CB with Human C5a Receptors This information is current as András N. Spaan, Ariën Schiepers, Carla J. C. de Haas, of October 1, 2021. Davy D. J. J. van Hooijdonk, Cédric Badiou, Hugues Contamin, François Vandenesch, Gérard Lina, Norma P. Gerard, Craig Gerard, Kok P. M. van Kessel, Thomas Henry and Jos A. G. van Strijp J Immunol 2015; 195:1034-1043; Prepublished online 19 June 2015; Downloaded from doi: 10.4049/jimmunol.1500604 http://www.jimmunol.org/content/195/3/1034 http://www.jimmunol.org/ Supplementary http://www.jimmunol.org/content/suppl/2015/06/19/jimmunol.150060 Material 4.DCSupplemental References This article cites 46 articles, 14 of which you can access for free at: http://www.jimmunol.org/content/195/3/1034.full#ref-list-1 Why The JI? Submit online. by guest on October 1, 2021 • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2015 by The American Association of Immunologists, Inc. -
The Buzz About ADP-Ribosylation Toxins from Paenibacillus Larvae, the Causative Agent of American Foulbrood in Honey Bees
toxins Review The Buzz about ADP-Ribosylation Toxins from Paenibacillus larvae, the Causative Agent of American Foulbrood in Honey Bees Julia Ebeling 1 , Anne Fünfhaus 1 and Elke Genersch 1,2,* 1 Department of Molecular Microbiology and Bee Diseases, Institute for Bee Research, 16540 Hohen Neuendorf, Germany; [email protected] (J.E.); [email protected] (A.F.) 2 Department of Veterinary Medicine, Institute of Microbiology and Epizootics, Freie Universität Berlin, 14163 Berlin, Germany * Correspondence: [email protected]; Tel.: +49-3303-293833 Abstract: The Gram-positive, spore-forming bacterium Paenibacillus larvae is the etiological agent of American Foulbrood, a highly contagious and often fatal honey bee brood disease. The species P. lar- vae comprises five so-called ERIC-genotypes which differ in virulence and pathogenesis strategies. In the past two decades, the identification and characterization of several P. larvae virulence factors have led to considerable progress in understanding the molecular basis of pathogen-host-interactions during P. larvae infections. Among these virulence factors are three ADP-ribosylating AB-toxins, Plx1, Plx2, and C3larvin. Plx1 is a phage-born toxin highly homologous to the pierisin-like AB-toxins expressed by the whites-and-yellows family Pieridae (Lepidoptera, Insecta) and to scabin expressed by the plant pathogen Streptomyces scabiei. These toxins ADP-ribosylate DNA and thus induce apoptosis. While the presumed cellular target of Plx1 still awaits final experimental proof, the classification of the A subunits of the binary AB-toxins Plx2 and C3larvin as typical C3-like toxins, which ADP-ribosylate Rho-proteins, has been confirmed experimentally.