The Adhesion and Invasion Mechanisms of Streptococci
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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]. -
Hemolysin from Escherichia Coli Uses Endogenous Amplification Through P2X Receptor Activation to Induce Hemolysis
␣-Hemolysin from Escherichia coli uses endogenous amplification through P2X receptor activation to induce hemolysis Marianne Skalsa, Niklas R. Jorgensenb, Jens Leipzigera, and Helle A. Praetoriusa,1 aDepartment of Physiology and Biophysics, Water and Salt Research Center, Aarhus University, Ole Worms Alle 1160, 8000 Aarhus C, Denmark; and bDepartment for Clinical Biochemistry, Roskilde Hospital, Koegevej 3-7, 4000 Roskilde, Denmark Edited by Sucharit Bhakdi, University of Mainz, Mainz, Germany, and accepted by the Editorial Board January 6, 2009 (received for review July 22, 2008) Escherichia coli is the dominant facultative bacterium in the normal and are referred to as P2X1–7. All P2X receptors are permeable to intestinal flora. E. coli is, however, also responsible for the majority small monovalent cations and some have significant calcium per- of serious extraintestinal infections. There are distinct serotypical meability (11). Here we show that human, murine, and equine differences between facultative and invasive E. coli strains. Inva- erythrocytes use a combination of P2X1 and P2X7 receptor acti- sive strains frequently produce virulence factors such as ␣-hemolysin vation for full HlyA-induced hemolysis to occur. This is particularly (HlyA), which causes hemolysis by forming pores in the erythrocyte interesting, as prolonged stimulation of P2X7 receptors are known membrane. The present study reveals that this pore formation to increase the plasma membrane permeability to an extent that triggers purinergic receptor activation to mediate the full hemo- eventually leads to lysis of certain cells (12). In macrophages it has lytic action. Non-selective ATP-receptor (P2) antagonists (PPADS, been shown that pannexin1, a recently discovered pore-forming suramin) and ATP scavengers (apyrase, hexokinase) concentration protein, is required for this increment in permeability (12, 13). -
Quercetin Inhibits Virulence Properties of Porphyromas Gingivalis In
www.nature.com/scientificreports OPEN Quercetin inhibits virulence properties of Porphyromas gingivalis in periodontal disease Zhiyan He1,2,3,7, Xu Zhang1,2,3,7, Zhongchen Song2,3,4, Lu Li5, Haishuang Chang6, Shiliang Li5* & Wei Zhou1,2,3* Porphyromonas gingivalis is a causative agent in the onset and progression of periodontal disease. This study aims to investigate the efects of quercetin, a natural plant product, on P. gingivalis virulence properties including gingipain, haemagglutinin and bioflm formation. Antimicrobial efects and morphological changes of quercetin on P. gingivalis were detected. The efects of quercetin on gingipains activities and hemolytic, hemagglutination activities were evaluated using chromogenic peptides and sheep erythrocytes. The bioflm biomass and metabolism with diferent concentrations of quercetin were assessed by the crystal violet and MTT assay. The structures and thickness of the bioflms were observed by confocal laser scanning microscopy. Bacterial cell surface properties including cell surface hydrophobicity and aggregation were also evaluated. The mRNA expression of virulence and iron/heme utilization was assessed using real time-PCR. Quercetin exhibited antimicrobial efects and damaged the cell structure. Quercetin can inhibit gingipains, hemolytic, hemagglutination activities and bioflm formation at sub-MIC concentrations. Molecular docking analysis further indicated that quercetin can interact with gingipains. The bioflm became sparser and thinner after quercetin treatment. Quercetin also modulate cell surface hydrophobicity and aggregation. Expression of the genes tested was down-regulated in the presence of quercetin. In conclusion, our study demonstrated that quercetin inhibited various virulence factors of P. gingivalis. Periodontal disease is a common chronic infammatory disease that characterized swelling and bleeding of the gums clinically, and leading to the progressive destruction of tooth-supporting tissues including the gingiva, alveolar bone, periodontal ligament, and cementum. -
Disposal of Toxin Heptamers by Extracellular Vesicle Formation and Lysosomal Degradation
toxins Article Major Determinants of Airway Epithelial Cell Sensitivity to S. aureus Alpha-Toxin: Disposal of Toxin Heptamers by Extracellular Vesicle Formation and Lysosomal Degradation Nils Möller 1,* , Sabine Ziesemer 1, Christian Hentschker 2, Uwe Völker 2 and Jan-Peter Hildebrandt 1 1 Animal Physiology and Biochemistry, University of Greifswald, Felix Hausdorff-Strasse 1, D-17489 Greifswald, Germany; [email protected] (S.Z.); [email protected] (J.-P.H.) 2 Department of Functional Genomics, Interfaculty Institute for Genetics and Functional Genomics, University Medicine Greifswald, Felix Hausdorff-Strasse 8, D-17475 Greifswald, Germany; [email protected] (C.H.); [email protected] (U.V.) * Correspondence: [email protected] Abstract: Alpha-toxin is a major virulence factor of Staphylococcus aureus. Monomer binding to host cell membranes results in the formation of heptameric transmembrane pores. Among human model airway epithelial cell lines, A549 cells were most sensitive toward the toxin followed by 16HBE14o- and S9 cells. In this study we investigated the processes of internalization of pore-containing plasma membrane areas as well as potential pathways for heptamer degradation (lysosomal, proteasomal) or disposal (formation of exosomes/micro-vesicles). The abundance of toxin heptamers upon applying an alpha-toxin pulse to the cells declined both in extracts of whole cells and of cellular membranes of Citation: Möller, N.; Ziesemer, S.; S9 cells, but not in those of 16HBE14o- or A549 cells. Comparisons of heptamer degradation rates un- Hentschker, C.; Völker, U.; der inhibition of lysosomal or proteasomal degradation revealed that an important route of heptamer Hildebrandt, J.-P. -
Streptococcus Agalactiae, Invasive (Group B Streptococcus)Rev Jan 2018
Streptococcus agalactiae, Invasive (Group B Streptococcus) Streptococcus agalactiae, Invasive (Group B Streptococcus) rev Jan 2018 BASIC EPIDEMIOLOGY Infectious Agent Streptococcus agalactiae (group B Streptococcus [GBS]) are beta-hemolytic, Gram-positive cocci. Transmission Transmission of group B Streptococcus from mother to infant occurs just before or during delivery. After delivery, infants are occasionally infected via person-to-person transmission in the nursery. In adults, GBS can be acquired through person-to-person transmission from healthy carriers (colonized but asymptomatic) in the community. Incubation Period The incubation period for early onset GBS disease in neonates is <7 days. The incubation period for late onset GBS disease in infants, children and adults is unknown. Communicability An estimated 10%–30% of women are carriers. GBS colonization occurs primarily in the gastrointestinal and genital tracts. Colonization is most often asymptomatic and does not require treatment. About half the infants born to colonized mothers are also colonized on the skin and mucosal surfaces as a result of passage through the birth canal or as a result of GBS ascending into the amniotic fluid. The majority of colonized infants, 98%, are asymptomatic. Clinical Illness In neonates two syndromes exist: early-onset disease (<7 days old) and late-onset disease (7-90 days old). Both syndromes can include sepsis, pneumonia and meningitis. Pregnancy-related infections include sepsis, amnionitis, urinary tract infection and stillbirth. In adults, pneumonia, bacteremia, meningitis, joint infections or soft tissue infections can occur. Severity The Centers for Disease Control and Prevention estimates that 0.53 deaths per 100,000 people occur annually. GBS is the leading cause of neonatal sepsis in the US. -
Transport Proteins Promoting Escherichia Coli Pathogenesis
Microbial Pathogenesis 71-72 (2014) 41e55 Contents lists available at ScienceDirect Microbial Pathogenesis journal homepage: www.elsevier.com/locate/micpath Transport proteins promoting Escherichia coli pathogenesis Fengyi Tang 1, Milton H. Saier Jr. * Department of Molecular Biology, Division of Biological Sciences, University of California at San Diego, La Jolla, CA 92093-0116, USA article info abstract Article history: Escherichia coli is a genetically diverse species infecting hundreds of millions of people worldwide Received 26 November 2013 annually. We examined seven well-characterized E. coli pathogens causing urinary tract infections, Received in revised form gastroenteritis, pyelonephritis and haemorrhagic colitis. Their transport proteins were identified and 19 March 2014 compared with each other and a non-pathogenic E. coli K12 strain to identify transport proteins related Accepted 20 March 2014 to pathogenesis. Each pathogen possesses a unique set of protein secretion systems for export to the cell Available online 18 April 2014 surface or for injecting effector proteins into host cells. Pathogens have increased numbers of iron siderophore receptors and ABC iron uptake transporters, but the numbers and types of low-affinity Keywords: Escherichia coli secondary iron carriers were uniform in all strains. The presence of outer membrane iron complex re- fi Pathogenesis ceptors and high-af nity ABC iron uptake systems correlated, suggesting co-evolution. Each pathovar Transporters encodes a different set of pore-forming toxins and virulence-related outer membrane proteins lacking in Toxins K12. Intracellular pathogens proved to have a characteristically distinctive set of nutrient uptake porters, Iron acquisition different from those of extracellular pathogens. The results presented in this report provide information Intra vs. -
N-Glycan Trimming in the ER and Calnexin/Calreticulin Cycle
Neurotransmitter receptorsGABA and A postsynapticreceptor activation signal transmission Ligand-gated ion channel transport GABAGABA Areceptor receptor alpha-5 alpha-1/beta-1/gamma-2 subunit GABA A receptor alpha-2/beta-2/gamma-2GABA receptor alpha-4 subunit GABAGABA receptor A receptor beta-3 subunitalpha-6/beta-2/gamma-2 GABA-AGABA receptor; A receptor alpha-1/beta-2/gamma-2GABA receptoralpha-3/beta-2/gamma-2 alpha-3 subunit GABA-A GABAreceptor; receptor benzodiazepine alpha-6 subunit site GABA-AGABA-A receptor; receptor; GABA-A anion site channel (alpha1/beta2 interface) GABA-A receptor;GABA alpha-6/beta-3/gamma-2 receptor beta-2 subunit GABAGABA receptorGABA-A receptor alpha-2receptor; alpha-1 subunit agonist subunit GABA site Serotonin 3a (5-HT3a) receptor GABA receptorGABA-C rho-1 subunitreceptor GlycineSerotonin receptor subunit3 (5-HT3) alpha-1 receptor GABA receptor rho-2 subunit GlycineGlycine receptor receptor subunit subunit alpha-2 alpha-3 Ca2+ activated K+ channels Metabolism of ingested SeMet, Sec, MeSec into H2Se SmallIntermediateSmall conductance conductance conductance calcium-activated calcium-activated calcium-activated potassium potassium potassiumchannel channel protein channel protein 2 protein 1 4 Small conductance calcium-activatedCalcium-activated potassium potassium channel alpha/beta channel 1 protein 3 Calcium-activated potassiumHistamine channel subunit alpha-1 N-methyltransferase Neuraminidase Pyrimidine biosynthesis Nicotinamide N-methyltransferase Adenosylhomocysteinase PolymerasePolymeraseHistidine basic -
Membrane Topology of the C. Elegans SEL-12 Presenilin
Neuron, Vol. 17, 1015±1021, November, 1996, Copyright 1996 by Cell Press Membrane Topology of the C. elegans SEL-12 Presenilin Xiajun Li* and Iva Greenwald*²³ [this issue of Neuron]; Thinakaran et al., 1996). In the *Integrated Program in Cellular, Molecular, Discussion, we examine the amino acid sequence in and Biophysical Studies light of the deduced topology. ² Department of Biochemistry and Molecular Biophysics Results ³ Howard Hughes Medical Institute Columbia University Sequence analysis suggests that SEL-12 and human College of Physicians and Surgeons presenilins have ten hydrophobic regions (Figure 1). In New York, New York 10032 this study, we provide evidence that a total of eight of these hydrophobic regions function as transmembrane domains in vivo. Below, we use the term ªhydrophobic Summary regionº to designate a segment of the protein with the potential to span the membrane, as inferred by hydro- Mutant presenilins cause Alzheimer's disease. Pre- phobicity analysis, and ªtransmembrane domainº to senilins have multiple hydrophobic regions that could designate a hydrophobic region that our data suggest theoretically span a membrane, and a knowledge of actually spans a membrane. the membrane topology is crucial for deducing the mechanism of presenilin function. By analyzing the activity of b-galactosidase hybrid proteins expressed Strategy in C. elegans, we show that the C. elegans SEL-12 We constructed transgenes encoding hybrid SEL- presenilin has eight transmembrane domains and that 12::LacZ proteins, in which LacZ was placed after each there is a cleavage site after the sixth transmembrane of ten hydrophobic regions identified by hydrophobicity domain. We examine the presenilin sequence in view analysis (see Figure 1). -
Molecular Mechanisms of Inhibition of Streptococcus Species by Phytochemicals
molecules Review Molecular Mechanisms of Inhibition of Streptococcus Species by Phytochemicals Soheila Abachi 1, Song Lee 2 and H. P. Vasantha Rupasinghe 1,* 1 Faculty of Agriculture, Dalhousie University, Truro, NS PO Box 550, Canada; [email protected] 2 Faculty of Dentistry, Dalhousie University, Halifax, NS PO Box 15000, Canada; [email protected] * Correspondence: [email protected]; Tel.: +1-902-893-6623 Academic Editors: Maurizio Battino, Etsuo Niki and José L. Quiles Received: 7 January 2016 ; Accepted: 6 February 2016 ; Published: 17 February 2016 Abstract: This review paper summarizes the antibacterial effects of phytochemicals of various medicinal plants against pathogenic and cariogenic streptococcal species. The information suggests that these phytochemicals have potential as alternatives to the classical antibiotics currently used for the treatment of streptococcal infections. The phytochemicals demonstrate direct bactericidal or bacteriostatic effects, such as: (i) prevention of bacterial adherence to mucosal surfaces of the pharynx, skin, and teeth surface; (ii) inhibition of glycolytic enzymes and pH drop; (iii) reduction of biofilm and plaque formation; and (iv) cell surface hydrophobicity. Collectively, findings from numerous studies suggest that phytochemicals could be used as drugs for elimination of infections with minimal side effects. Keywords: streptococci; biofilm; adherence; phytochemical; quorum sensing; S. mutans; S. pyogenes; S. agalactiae; S. pneumoniae 1. Introduction The aim of this review is to summarize the current knowledge of the antimicrobial activity of naturally occurring molecules isolated from plants against Streptococcus species, focusing on their mechanisms of action. This review will highlight the phytochemicals that could be used as alternatives or enhancements to current antibiotic treatments for Streptococcus species. -
Beta-Haemolytic Streptococci (BHS)
technical sheet Beta-Haemolytic Streptococci (BHS) Classification Transmission Gram-positive cocci, often found in chains Transmission is generally via direct contact with nasopharyngeal secretions from ill or carrier animals. Family Animals may also be infected by exposure to ill or Streptococcaceae carrier caretakers. β-haemolytic streptococci are characterized by Lancefield grouping (a characterization based on Clinical Signs and Lesions carbohydrates in the cell walls). Only some Lancefield In mice and rats, generally none. Occasional groups are of clinical importance in laboratory rodents. outbreaks of disease associated with BHS are Streptococci are generally referred to by their Lancefield reported anecdotally and in the literature. In most grouping but genus and species are occasionally used. cases described, animals became systemically ill after experimental manipulation, and other animals Group A: Streptococcus pyogenes in the colony were found to be asymptomatic Group B: Streptococcus agalactiae carriers. In a case report not involving experimental Group C: Streptococcus equi subsp. zooepidemicus manipulation, DBA/2NTac mice and their hybrids were Group G: Streptococcus canis more susceptible to an ascending pyelonephritis and subsequent systemic disease induced by Group B Affected species streptococci than other strains housed in the same β-haemolytic streptococci are generally considered barrier. opportunists that can colonize most species. Mice and guinea pigs are reported most frequently with clinical In guinea pigs, infection with Group C streptococci signs, although many rodent colonies are colonized leads to swelling and infection of the lymph nodes. with no morbidity, suggesting disease occurs only with Guinea pigs can be inapparent carriers of the organism severe stress or in other exceptional circumstances. -
The Microbiology of Impetigo in Indigenous Children: Associations Between Streptococcus Pyogenes, Staphylococcus Aureus, Scabies
Bowen et al. BMC Infectious Diseases DOI 10.1186/s12879-014-0727-5 RESEARCH ARTICLE Open Access The microbiology of impetigo in Indigenous children: associations between Streptococcus pyogenes, Staphylococcus aureus, scabies, and nasal carriage Asha C Bowen1,2,3*, Steven YC Tong1,4, Mark D Chatfield3 and Jonathan R Carapetis2,3 Abstract Background: Impetigo is caused by both Streptococcus pyogenes and Staphylococcus aureus; the relative contributions of each have been reported to fluctuate with time and region. While S. aureus is reportedly on the increase in most industrialised settings, S. pyogenes is still thought to drive impetigo in endemic, tropical regions. However, few studies have utilised high quality microbiological culture methods to confirm this assumption. We report the prevalence and antimicrobial resistance of impetigo pathogens recovered in a randomised, controlled trial of impetigo treatment conducted in remote Indigenous communities of northern Australia. Methods: Each child had one or two sores, and the anterior nares, swabbed. All swabs were transported in skim milk tryptone glucose glycogen broth and frozen at –70°C, until plated on horse blood agar. S. aureus and S. pyogenes were confirmed with latex agglutination. Results: From 508 children, we collected 872 swabs of sores and 504 swabs from the anterior nares prior to commencement of antibiotic therapy. S. pyogenes and S. aureus were identified together in 503/872 (58%) of sores; with an additional 207/872 (24%) sores having S. pyogenes and 81/872 (9%) S. aureus, in isolation. Skin sore swabs taken during episodes with a concurrent diagnosis of scabies were more likely to culture S. -
Tailored Liposomal Nanotraps for the Treatment of Streptococcal Infections
Besançon et al. J Nanobiotechnol (2021) 19:46 https://doi.org/10.1186/s12951-021-00775-x Journal of Nanobiotechnology RESEARCH Open Access Tailored liposomal nanotraps for the treatment of Streptococcal infections Hervé Besançon1 , Viktoriia Babiychuk1, Yu Larpin1, René Köfel1, Dominik Schittny1, Lara Brockhus1, Lucy J. Hathaway2, Parham Sendi2, Annette Draeger1^ and Eduard Babiychuk1* Abstract Background: Streptococcal infections are associated with life-threatening pneumonia and sepsis. The rise in anti- biotic resistance calls for novel approaches to treat bacterial diseases. Anti-virulence strategies promote a natural way of pathogen clearance by eliminating the advantage provided to bacteria by their virulence factors. In contrast to antibiotics, anti-virulence agents are less likely to exert selective evolutionary pressure, which is a prerequisite for the development of drug resistance. As part of their virulence mechanism, many bacterial pathogens secrete cytol- ytic exotoxins (hemolysins) that destroy the host cell by destabilizing their plasma membrane. Liposomal nanotraps, mimicking plasmalemmal structures of host cells that are specifcally targeted by bacterial toxins are being developed in order to neutralize-by competitive sequestration-numerous exotoxins. Results: In this study, the liposomal nanotrap technology is further developed to simultaneously neutralize the whole palette of cytolysins produced by Streptococcus pneumoniae, Streptococcus pyogenes and Streptococcus dys- galactiae subspecies equisimilis-pathogens that