M1 protein allows Group A streptococcal survival in phagocyte extracellular traps through cathelicidin inhibition.
about
Neutrophil extracellular traps contain calprotectin, a cytosolic protein complex involved in host defense against Candida albicansAntimicrobial Activity of Mast Cells: Role and Relevance of Extracellular DNA TrapsInteraction of Bacterial Exotoxins with Neutrophil Extracellular Traps: Impact for the Infected HostStrategies and molecular tools to fight antimicrobial resistance: resistome, transcriptome, and antimicrobial peptidesAntibiotic development challenges: the various mechanisms of action of antimicrobial peptides and of bacterial resistanceModulation of neutrophil NETosis: interplay between infectious agents and underlying host physiology.Mast cells and neutrophils release IL-17 through extracellular trap formation in psoriasisMolecular and genomic characterization of pathogenic traits of group A Streptococcus pyogenesRole for streptococcal collagen-like protein 1 in M1T1 group A Streptococcus resistance to neutrophil extracellular trapsCoiled-coil irregularities of the M1 protein structure promote M1-fibrinogen interaction and influence group A Streptococcus host cell interactions and virulence.ETosis: A Microbicidal Mechanism beyond Cell Death.Neutrophil extracellular traps: is immunity the second function of chromatin?Bacteria fighting back: how pathogens target and subvert the host innate immune system.M1T1 group A streptococcal pili promote epithelial colonization but diminish systemic virulence through neutrophil extracellular entrapment.Extracellular traps are associated with human and mouse neutrophil and macrophage mediated killing of larval Strongyloides stercoralis.Neutrophil extracellular trap (NET)-mediated killing of Pseudomonas aeruginosa: evidence of acquired resistance within the CF airway, independent of CFTR.M protein and hyaluronic acid capsule are essential for in vivo selection of covRS mutations characteristic of invasive serotype M1T1 group A Streptococcus.Dying for a cause: NETosis, mechanisms behind an antimicrobial cell death modalityNuclease expression by Staphylococcus aureus facilitates escape from neutrophil extracellular traps.Novel role of the antimicrobial peptide LL-37 in the protection of neutrophil extracellular traps against degradation by bacterial nucleases.Neutrophil elastase and myeloperoxidase regulate the formation of neutrophil extracellular traps.A bacterial pathogen co-opts host plasmin to resist killing by cathelicidin antimicrobial peptidesAntibacterial activity of the contact and complement systems is blocked by SIC, a protein secreted by Streptococcus pyogenesAntimicrobial Peptide Resistance Mechanisms of Gram-Positive Bacteria.Factor H binds to the hypervariable region of many Streptococcus pyogenes M proteins but does not promote phagocytosis resistance or acute virulence.The human antimicrobial peptide LL-37 binds directly to CsrS, a sensor histidine kinase of group A Streptococcus, to activate expression of virulence factors.Streptococcal inhibitor of complement promotes innate immune resistance phenotypes of invasive M1T1 group A StreptococcusBeta-Lactamase Repressor BlaI Modulates Staphylococcus aureus Cathelicidin Antimicrobial Peptide Resistance and VirulenceStreptococcus pyogenes Sortase Mutants Are Highly Susceptible to Killing by Host Factors Due to Aberrant Envelope PhysiologyCationic antimicrobial peptide resistance mechanisms of streptococcal pathogens.Conquering Neutrophils.Group A Streptococcal M1 Protein Sequesters Cathelicidin to Evade Innate Immune KillingA NET Outcome.Characterization of streptokinases from group A Streptococci reveals a strong functional relationship that supports the coinheritance of plasminogen-binding M protein and cluster 2b streptokinase.Host-protective effect of circulating pentraxin 3 (PTX3) and complex formation with neutrophil extracellular traps.Activation of PAD4 in NET formation.Study of streptococcal hemoprotein receptor (Shr) in iron acquisition and virulence of M1T1 group A streptococcus.Immunomodulatory Role of Clarithromycin in Acinetobacter baumannii Infection via Formation of Neutrophil Extracellular TrapsDifferential neutrophil responses to bacterial stimuli: Streptococcal strains are potent inducers of heparin-binding protein and resistin-releaseExtracellular traps and macrophages: new roles for the versatile phagocyte.
P2860
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P2860
M1 protein allows Group A streptococcal survival in phagocyte extracellular traps through cathelicidin inhibition.
description
2009 nî lūn-bûn
@nan
2009年の論文
@ja
2009年論文
@yue
2009年論文
@zh-hant
2009年論文
@zh-hk
2009年論文
@zh-mo
2009年論文
@zh-tw
2009年论文
@wuu
2009年论文
@zh
2009年论文
@zh-cn
name
M1 protein allows Group A stre ...... rough cathelicidin inhibition.
@ast
M1 protein allows Group A stre ...... rough cathelicidin inhibition.
@en
type
label
M1 protein allows Group A stre ...... rough cathelicidin inhibition.
@ast
M1 protein allows Group A stre ...... rough cathelicidin inhibition.
@en
prefLabel
M1 protein allows Group A stre ...... rough cathelicidin inhibition.
@ast
M1 protein allows Group A stre ...... rough cathelicidin inhibition.
@en
P2093
P2860
P50
P356
P1476
M1 protein allows Group A stre ...... rough cathelicidin inhibition.
@en
P2093
Bernard Beall
Case W McNamara
Maren von Köckritz-Blickwede
Partho Ghosh
Sandra Myskowski
Xavier Lauth
P2860
P304
P356
10.1159/000203645
P577
2009-02-20T00:00:00Z