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Related Experiment Videos

Apoptosis driven infection.

G van Zandbergen1, W Solbach, T Laskay

  • 1Institute for Medical Microbiology and Hygiene, Centre for Structural and Cell Biology in Medicine, University of Lübeck, Lübeck, Germany. Zandbergen@uni-luebeck.de

Autoimmunity
|May 23, 2007
PubMed
Summary
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Certain pathogens, like Leishmania major, exploit the "eat me" signal phosphatidylserine (PS) to evade immune cells. This allows silent invasion of phagocytes, such as neutrophils and macrophages, establishing infection.

Area of Science:

  • Immunology
  • Microbiology
  • Cell Biology

Background:

  • Professional phagocytes, including polymorphonuclear neutrophil granulocytes (PMN) and macrophages (MF), are crucial for pathogen elimination.
  • Microorganisms have evolved strategies to evade phagocytic killing and establish infection within host cells.
  • Apoptotic cells utilize phosphatidylserine (PS) exposure as an 'eat me' signal, suppressing immune responses during phagocytosis.

Purpose of the Study:

  • To investigate the evasion strategies of Leishmania major, a prototypic intracellular pathogen.
  • To elucidate how pathogens utilize the apoptotic 'eat me' signal, PS, for host cell invasion.
  • To discuss other pathogens employing PS for infection establishment.

Main Methods:

  • Focus on Leishmania major as a model organism.

Related Experiment Videos

  • Analysis of PS exposure by pathogens and infected host cells.
  • Observational study of pathogen entry into PMN and MF.

    • Main Results:

    • Leishmania major utilizes PS to silently enter PMN, facilitating the survival of viable parasites.
    • Infected PMN expose PS, enabling Leishmania major to silently invade MF, their definitive host cells.
    • PS acts as a critical molecular mimicry signal for immune evasion.

    Conclusions:

    • Leishmania major employs PS-mediated immune silencing for successful infection.
    • The apoptotic 'eat me' signal PS is a conserved mechanism exploited by various pathogens.
    • Targeting PS-mediated pathways could offer novel therapeutic strategies against intracellular infections.