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We began analyzing https://link.springer.com/article/10.1007/s00109-009-0566-9, but it redirected us to https://link.springer.com/article/10.1007/s00109-009-0566-9. The analysis below is for the second page.

Title[redir]:
M1T1 group A streptococcal pili promote epithelial colonization but diminish systemic virulence through neutrophil extracellular entrapment | Journal of Molecular Medicine
Description:
Group A Streptococcus is a leading human pathogen associated with a diverse array of mucosal and systemic infections. Cell wall anchored pili were recently described in several species of pathogenic streptococci, and in the case of GAS, these surface appendages were demonstrated to facilitate epithelial cell adherence. Here we use targeted mutagenesis to evaluate the contribution of pilus expression to virulence of the globally disseminated M1T1 GAS clone, the leading agent of both GAS pharyngitis and severe invasive infections. We confirm that pilus expression promotes GAS adherence to pharyngeal cells, keratinocytes, and skin. However, in contrast to findings reported for group B streptococcal and pneumococcal pili, we observe that pilus expression reduces GAS virulence in murine models of necrotizing fasciitis, pneumonia and sepsis, while decreasing GAS survival in human blood. Further analysis indicated the systemic virulence attenuation associated with pilus expression was not related to differences in phagocytic uptake, complement deposition or cathelicidin antimicrobial peptide sensitivity. Rather, GAS pili were found to induce neutrophil IL-8 production, promote neutrophil transcytosis of endothelial cells, and increase neutrophil release of DNA-based extracellular traps, ultimately promoting GAS entrapment and killing within these structures.

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  • Politics
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Custom-built

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Traffic Estimate {šŸ“ˆ}

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šŸ™ļø Massive Traffic: 50M - 100M visitors per month


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Keywords {šŸ”}

gas, Γpil, mutant, article, pilus, google, scholar, pubmed, human, cas, pili, group, neutrophil, expression, adherence, skin, streptococcus, fig, killing, virulence, infection, neutrophils, bacteria, complemented, spy, nets, extracellular, pil, streptococcal, mice, nizet, cell, strain, mouse, cfu, epithelial, cells, min, incubated, net, invasive, disease, plated, added, surface, assays, role, blood, pbs, diluted,

Topics {āœ’ļø}

hematoxylin-eosin-stained lung sections cytokine-induced neutrophil-derived interleukin-8 von kƶckritz-blickwede dna-based extracellular traps representative hematoxylin–eosin-staining article download pdf full-length gas pili Ī“pil + pil complemented strain Ī“pil + pil complemented strains full-length spy0128 gene monocyte-derived peptide agonist Ī“pil + pil complemented mutant il-8 protease spycep/scpc neutrophil extracellular traps knockout vector pspy1028-ko live/dead baclight staining Ī“pil + pil gas compared 1Ā mm zirconia/silica beads phagocyte extracellular traps host inflammatory responses gram-positive bacteria including potentially life-threatening pneumonia produce life-threatening infections significantly smaller lesions innate immune-mediated selection mentioned net-resistance genes fitc-labeled gas adherent streptococcus pyogenes disease fitc-labeled gas entrapped open access promote neutrophil transcytosis full access major pilus subunit cell lines representative collagen-binding protein [12] neutrophil extracellular entrapment innate immune system expression profile related subjects phage-encoded dnase sda1 increases gas entrapment 5 × 104Ā cfu logarithmic-phase gas streptococcus produce pilus pilus backbone subunit gas pilus expression streptococcus promotes resistance stimulate bactericidal activities major epithelial surfaces cell death pathway gas m1t1 pilus

Schema {šŸ—ŗļø}

WebPage:
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         headline:M1T1 group A streptococcal pili promote epithelial colonization but diminish systemic virulence through neutrophil extracellular entrapment
         description:Group A Streptococcus is a leading human pathogen associated with a diverse array of mucosal and systemic infections. Cell wall anchored pili were recently described in several species of pathogenic streptococci, and in the case of GAS, these surface appendages were demonstrated to facilitate epithelial cell adherence. Here we use targeted mutagenesis to evaluate the contribution of pilus expression to virulence of the globally disseminated M1T1 GAS clone, the leading agent of both GAS pharyngitis and severe invasive infections. We confirm that pilus expression promotes GAS adherence to pharyngeal cells, keratinocytes, and skin. However, in contrast to findings reported for group B streptococcal and pneumococcal pili, we observe that pilus expression reduces GAS virulence in murine models of necrotizing fasciitis, pneumonia and sepsis, while decreasing GAS survival in human blood. Further analysis indicated the systemic virulence attenuation associated with pilus expression was not related to differences in phagocytic uptake, complement deposition or cathelicidin antimicrobial peptide sensitivity. Rather, GAS pili were found to induce neutrophil IL-8 production, promote neutrophil transcytosis of endothelial cells, and increase neutrophil release of DNA-based extracellular traps, ultimately promoting GAS entrapment and killing within these structures.
         datePublished:2009-12-04T00:00:00Z
         dateModified:2009-12-04T00:00:00Z
         pageStart:371
         pageEnd:381
         license:https://creativecommons.org/licenses/by-nc/2.0
         sameAs:https://doi.org/10.1007/s00109-009-0566-9
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            Pilus
            Virulence factor
            IL-8
            Neutrophil extracellular traps
            Molecular Medicine
            Human Genetics
            Internal Medicine
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                        name:Department of Pediatrics, University of California San Diego, La Jolla, USA
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                     name:Rady Children’s Hospital
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ScholarlyArticle:
      headline:M1T1 group A streptococcal pili promote epithelial colonization but diminish systemic virulence through neutrophil extracellular entrapment
      description:Group A Streptococcus is a leading human pathogen associated with a diverse array of mucosal and systemic infections. Cell wall anchored pili were recently described in several species of pathogenic streptococci, and in the case of GAS, these surface appendages were demonstrated to facilitate epithelial cell adherence. Here we use targeted mutagenesis to evaluate the contribution of pilus expression to virulence of the globally disseminated M1T1 GAS clone, the leading agent of both GAS pharyngitis and severe invasive infections. We confirm that pilus expression promotes GAS adherence to pharyngeal cells, keratinocytes, and skin. However, in contrast to findings reported for group B streptococcal and pneumococcal pili, we observe that pilus expression reduces GAS virulence in murine models of necrotizing fasciitis, pneumonia and sepsis, while decreasing GAS survival in human blood. Further analysis indicated the systemic virulence attenuation associated with pilus expression was not related to differences in phagocytic uptake, complement deposition or cathelicidin antimicrobial peptide sensitivity. Rather, GAS pili were found to induce neutrophil IL-8 production, promote neutrophil transcytosis of endothelial cells, and increase neutrophil release of DNA-based extracellular traps, ultimately promoting GAS entrapment and killing within these structures.
      datePublished:2009-12-04T00:00:00Z
      dateModified:2009-12-04T00:00:00Z
      pageStart:371
      pageEnd:381
      license:https://creativecommons.org/licenses/by-nc/2.0
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         Pilus
         Virulence factor
         IL-8
         Neutrophil extracellular traps
         Molecular Medicine
         Human Genetics
         Internal Medicine
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                     type:PostalAddress
                  type:Organization
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                     name:Department of Pediatrics, University of California San Diego, La Jolla, USA
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                     type:PostalAddress
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            name:Victor Nizet
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                     type:PostalAddress
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                  name:University of California San Diego
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      name:Anjuli M. Timmer
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            name:University of California San Diego
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            address:
               name:Department of Pediatrics, University of California San Diego, La Jolla, USA
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            name:University Medical Center Utrecht
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      name:Richard L. Gallo
      affiliation:
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            address:
               name:Division of Dermatology, University of California San Diego, La Jolla, USA
               type:PostalAddress
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            name:VA San Diego Health Care System
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               type:PostalAddress
            type:Organization
      name:Maren von Kƶckritz-Blickwede
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            name:University of California San Diego
            address:
               name:Department of Pediatrics, University of California San Diego, La Jolla, USA
               type:PostalAddress
            type:Organization
      name:Victor Nizet
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            name:University of California San Diego
            address:
               name:Department of Pediatrics, University of California San Diego, La Jolla, USA
               type:PostalAddress
            type:Organization
            name:University of California San Diego
            address:
               name:Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California San Diego, La Jolla, USA
               type:PostalAddress
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            name:Rady Children’s Hospital
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               name:Rady Children’s Hospital, San Diego, USA
               type:PostalAddress
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      name:Department of Pediatrics, University of California San Diego, La Jolla, USA
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      name:Department of Pediatrics, University of California San Diego, La Jolla, USA
      name:Department of Pediatrics, University of California San Diego, La Jolla, USA
      name:Department of Pediatrics, University of California San Diego, La Jolla, USA
      name:Medical Microbiology, University Medical Center Utrecht, Utrecht, Netherlands
      name:Division of Dermatology, University of California San Diego, La Jolla, USA
      name:VA San Diego Health Care System, San Diego, USA
      name:Department of Pediatrics, University of California San Diego, La Jolla, USA
      name:Department of Pediatrics, University of California San Diego, La Jolla, USA
      name:Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California San Diego, La Jolla, USA
      name:Rady Children’s Hospital, San Diego, USA

External Links {šŸ”—}(290)

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