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Related Concept Videos

Types of Toxins01:36

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Humans continually engage with an environment rich in potentially harmful chemicals. These are introduced to our bodies through inhalation, ingestion, or skin contact. These chemicals exist in various forms, such as air and environmental pollutants, agricultural chemicals, organic solvents, and heavy metals.
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Development and Assessment of Intracellular Infection Models for Staphylococcus aureus
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Staphylococcus aureus alpha toxin activates Notch in vascular cells.

Sonia L Hernandez1, Mildred Nelson2, Georgia R Sampedro3

  • 1Section of Pediatric Surgery, Department of Surgery, The University of Chicago, Chicago, IL, USA. soniah@uchicago.edu.

Angiogenesis
|October 17, 2018
PubMed
Summary

Staphylococcus aureus hemolysin alpha toxin (Hla) activates Notch signaling in vascular cells, potentially contributing to infection pathology. This discovery highlights a new mechanism in bacterial pathogenesis and vascular response.

Keywords:
Alpha-toxinHUVECNotchStaphylococcus aureus

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Area of Science:

  • Vascular Biology
  • Microbiology
  • Cell Signaling

Background:

  • Staphylococcus aureus infections cause significant morbidity, exacerbated by antibiotic resistance.
  • The toxin hemolysin alpha toxin (Hla) uses ADAM10 to mediate effects and is linked to Notch signaling.
  • Notch signaling regulates angiogenesis and is crucial in vascular and perivascular cells.

Purpose of the Study:

  • To investigate if Staphylococcus aureus Hla activates Notch signaling in vascular cells.
  • To elucidate the role of ADAM10 and γ-secretase in Hla-mediated Notch activation.
  • To explore the in vivo relevance of Hla-induced Notch activation during S. aureus infection.

Main Methods:

  • In vitro studies using human umbilical vein endothelial cells treated with recombinant Hla.
  • Luciferase assays, immunocytochemistry, and Western blotting to assess Notch activation.
  • In vivo studies using Notch reporter mice (retinal EC, aortic rings, skin inoculation) and human liver tissue analysis.

Main Results:

  • Recombinant Hla significantly increased Notch activation in endothelial cells, dependent on ADAM10 and γ-secretase.
  • Hla induced Notch activation in mouse retinal EC, aortic tip cells during sprouting, and skin post-infection.
  • Human liver tissue from S. aureus infected patients showed elevated Notch expression in vascular and perivascular cells.

Conclusions:

  • Staphylococcus aureus Hla toxin potently activates Notch signaling in vascular cells.
  • This Hla-mediated Notch activation may play a role in the pathobiology of S. aureus infections.
  • The findings suggest a novel mechanism linking bacterial toxins to host vascular signaling pathways.