scholarly journals High avidity drives the interaction between the streptococcal C1 phage endolysin, PlyC, with the cell surface carbohydrates of Group A Streptococcus

2021 ◽  
Author(s):  
Sebastian S. Broendum ◽  
Daniel E. Williams ◽  
Brooke K. Hayes ◽  
Felix Kraus ◽  
James Fodor ◽  
...  
Keyword(s):  
Cell Surface ◽  
Group A Streptococcus ◽  
High Avidity ◽  
Group A ◽  
Surface Carbohydrates

scholarly journals Assessing the Role of Pharyngeal Cell Surface Glycans in Group A Streptococcus Biofilm Formation

Antibiotics ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 775
Author(s):  
Heema K. N. Vyas ◽  
Anuk D. Indraratna ◽  
Arun Everest-Dass ◽  
Nicolle H. Packer ◽  
David M. P. De Oliveira ◽  
...  
Keyword(s):  
Sialic Acid ◽  
Cell Surface ◽  
Treatment Failure ◽  
Antibiotic Treatment ◽  
Biofilm Formation ◽  
Extracellular Polymeric Substances ◽  
Group A Streptococcus ◽  
Sialic Acid Residue ◽  
Group A ◽  
Terminal Mannose

Group A Streptococcus (GAS) causes 700 million infections and accounts for half a million deaths per year. Antibiotic treatment failure rates of 20–40% have been observed. The role host cell glycans play in GAS biofilm formation in the context of GAS pharyngitis and subsequent antibiotic treatment failure has not been previously investigated. GAS serotype M12 GAS biofilms were assessed for biofilm formation on Detroit 562 pharyngeal cell monolayers following enzymatic removal of all N-linked glycans from pharyngeal cells with PNGase F. Removal of N-linked glycans resulted in an increase in biofilm biomass compared to untreated controls. Further investigation into the removal of terminal mannose and sialic acid residues with α1-6 mannosidase and the broad specificity sialidase (Sialidase A) also found that biofilm biomass increased significantly when compared to untreated controls. Increases in biofilm biomass were associated with increased production of extracellular polymeric substances (EPS). Furthermore, it was found that M12 GAS biofilms grown on untreated pharyngeal monolayers exhibited a 2500-fold increase in penicillin tolerance compared to planktonic GAS. Pre-treatment of monolayers with exoglycosidases resulted in a further doubling of penicillin tolerance in resultant biofilms. Lastly, an additional eight GAS emm-types were assessed for biofilm formation in response to terminal mannose and sialic acid residue removal. As seen for M12, biofilm biomass on monolayers increased following removal of terminal mannose and sialic acid residues. Collectively, these data demonstrate that pharyngeal cell surface glycan structures directly impact GAS biofilm formation in a strain and glycan specific fashion.

scholarly journals Identification and Characterization of an Antigen I/II Family Protein Produced by Group A Streptococcus

2006 ◽  
Vol 74 (7) ◽  
pp. 4200-4213 ◽  
Author(s):  
Shizhen Zhang ◽  
Nicole M. Green ◽  
Izabela Sitkiewicz ◽  
Rance B. LeFebvre ◽  
James M. Musser
Keyword(s):  
Cell Surface ◽  
Group A Streptococcus ◽  
Bacterial Pathogen ◽  
Severe Infection ◽  
Genomic Islands ◽  
Oral Streptococci ◽  
Group B Streptococci ◽  
Gram Positive ◽  
Group A

ABSTRACT Group A Streptococcus (GAS) is a gram-positive human bacterial pathogen that causes infections ranging in severity from pharyngitis to life-threatening invasive disease, such as necrotizing fasciitis. Serotype M28 strains are consistently isolated from invasive infections, particularly puerperal sepsis, a severe infection that occurs during or after childbirth. We recently sequenced the genome of a serotype M28 GAS strain and discovered a novel 37.4-kb foreign genetic element designated region of difference 2 (RD2). RD2 is similar in gene content and organization to genomic islands found in group B streptococci (GBS), the major cause of neonatal infections. RD2 encodes seven proteins with conventional gram-positive secretion signal sequences, six of which have not been characterized. Herein, we report that one of these six proteins (M28_Spy1325; Spy1325) is a member of the antigen I/II family of cell surface-anchored molecules produced by oral streptococci. PCR and DNA sequence analysis found that Spy1325 is very well conserved in GAS strains of distinct M protein serotypes. As assessed by real-time TaqMan quantitative PCR, the Spy1325 gene was expressed in vitro, and Spy1325 protein was present in culture supernatants and on the GAS cell surface. Western immunoblotting and enzyme-linked immunosorbent assays indicated that Spy1325 was produced by GAS in infected mice and humans. Importantly, the immunization of mice with recombinant Spy1325 fragments conferred protection against GAS-mediated mortality. Similar to other antigen I/II proteins, recombinant Spy1325 bound purified human salivary agglutinin glycoprotein. Spy1325 may represent a shared virulence factor among GAS, GBS, and oral streptococci.

scholarly journals Investigating the functional relationship between streptokinase variants from Group A Streptococcus, and associated M-like proteins

2020 ◽  
Vol 2 (7A) ◽  
Author(s):  
Sophie Cherrington ◽  
Azhar Maqbool ◽  
Helen Philippou ◽  
Craig Thelwell
Keyword(s):  
Cell Surface ◽  
Group A Streptococcus ◽  
Fold Increase ◽  
Plasminogen Activation ◽  
Chromogenic Assay ◽  
Microtiter Plates ◽  
Fibrinogen Binding ◽  
Distinct Disease ◽  
Group A ◽  
Cluster 2

Background: Streptokinase (SK) from Group A streptococcus (GAS) activates human plasminogen to generate plasmin, which degrades fibrin clots tofacilitate bacterial dissemination. Sequence variants of SK from diverse GAS strains form distinct evolutionary clusters.Unlike cluster 1 SK, cluster 2 variants have very little activity in solution and depend on co-factors (e.g. fibrin(ogen)).Cluster 2 SK variants also appear to correlate with cell-surface M-like proteins: SK2a with M1 (fibrinogen-binding) and SK2b with PAM (plasminogen-binding). Methods: Plasminogen activation by recombinant SKs (rSK2a, rSK2b) was investigated by chromogenic assay; nickel-coated microtiter plates were used to immobilise recombinant M proteins (rPAM and rM1) via a C–terminal His tag to mimic cell surface plasmin generation. Results: Plasminogen activation by rSK2b is stimulated ∼18-fold by rPAM in solution; when rPAM is immobilised stimulation exceeds 100-fold. Fibrin is the most potent stimulator of rSK2a activity (7-fold increase) compared to fibrinogen (4-fold); when rM1 was included, either in solution or immobilised, there was no further stimulation of rSK2a activity with fibrinogen. Discussion: Stimulation ofSK2b activity by plasminogen bound to immobilised PAM suggests an important role for cell-surface plasmin generation. SK2a activity appears to be independent of M1, targeting fibrin directly. SK variants are commonly associated with distinct disease manifestations with SK2b commonly expressed by invasive skin-tropic strains of GAS and SK2a by nasopharynx-tropic strains. An improved understanding of the molecular mechanism of action by GAS SK variants may help to identify potential novel therapeutic targets for the treatment of invasive GAS diseases.

scholarly journals Surface Analyses and Immune Reactivities of Major Cell Wall-Associated Proteins of Group A Streptococcus

2005 ◽  
Vol 73 (5) ◽  
pp. 3137-3146 ◽  
Author(s):  
Jason N. Cole ◽  
Ruben D. Ramirez ◽  
Bart J. Currie ◽  
Stuart J. Cordwell ◽  
Steven P. Djordjevic ◽  
...  
Keyword(s):  
Cell Wall ◽  
Cell Surface ◽  
Streptococcus Pyogenes ◽  
Proteomic Analysis ◽  
Group A Streptococcus ◽  
Gas Cell ◽  
Distinct Cell ◽  
Associated Proteins ◽  
Group A

ABSTRACT A proteomic analysis was undertaken to identify cell wall-associated proteins of Streptococcus pyogenes. Seventy-four distinct cell wall-associated proteins were identified, 66 of which were novel. Thirty-three proteins were immunoreactive with pooled S. pyogenes-reactive human antisera. Biotinylation of the GAS cell surface identified 23 cell wall-associated proteins that are surface exposed.

scholarly journals Hypervirulent group A Streptococcus emergence in an acaspular background is associated with marked remodeling of the bacterial cell surface

PLoS ONE ◽  
2018 ◽  
Vol 13 (12) ◽  
pp. e0207897 ◽  
Author(s):  
Jessica Galloway-Peña ◽  
Sruti DebRoy ◽  
Chelcy Brumlow ◽  
Xiqi Li ◽  
Truc T. Tran ◽  
...  
Keyword(s):  
Cell Surface ◽  
Bacterial Cell ◽  
Group A Streptococcus ◽  
Bacterial Cell Surface ◽  
Group A

Etiology, clinical presentation, laboratory diagnostics, pathogenesis of impetigo and treatment methods

2020 ◽  
pp. 64-70
Author(s):  
Anastasiya Laknitskaya
Keyword(s):  
Streptococcus Pyogenes ◽  
Skin Diseases ◽  
Group A Streptococcus ◽  
Antibiotic Sensitivity ◽  
Antioxidant Defense System ◽  
Laboratory Diagnostics ◽  
Treatment Methods ◽  
Group A ◽  
The Individual

Currently, one of the priority medical and social problems is the optimization of treatment methods for pyoderma associated with Streptococcus pyogenes — group A streptococcus (GAS). To date, the proportion of pyoderma, the etiological factor of which is Streptococcus pyogenes, is about 6 % of all skin diseases and is in the range from 17.9 to 43.9 % of all dermatoses. Role of the bacterial factor in the development of streptococcal pyoderma is obvious. Traditional treatment complex includes antibacterial drugs selected individually, taking into account the antibiotic sensitivity of pathognomonic bacteria, and it is not always effective. Currently implemented immunocorrection methods often do not take into account specific immunological features of the disease, the individual, and the fact that the skin performs the function of not only a mechanical barrier, but it is also an immunocompetent organ. Such an approach makes it necessary to conduct additional studies clarifying the role of factors of innate and adaptive immunity, intercellular mediators and antioxidant defense system, that allow to optimize the treatment of this pathology.

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