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Related Concept Videos

Defense Against Bacterial Pathogens01:31

Defense Against Bacterial Pathogens

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The human immune system is a complex network of cells, tissues, and organs that work together to defend the body against bacterial infections. It consists of various immune cells, each playing a specific role in the defense mechanism.
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Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
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The innate immune response is an immediate and non-specific response against pathogens, acting swiftly to prevent the spread of infections. The primary cells involved in this response are phagocytes and natural killer (NK) cells.
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Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
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Related Experiment Video

Updated: Sep 28, 2025

Quantifying the Cytotoxicity of Staphylococcus aureus Against Human Polymorphonuclear Leukocytes
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Quantifying the Cytotoxicity of Staphylococcus aureus Against Human Polymorphonuclear Leukocytes

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Staphylococcus aureus Multiplexes Death-Effector Deoxyribonucleosides to Neutralize Phagocytes.

Eshraq Tantawy1,2, Nicoletta Schwermann1,2, Tjorven Ostermeier1,2

  • 1Research Group Pathogenesis of Bacterial Infections, TWINCORE, Centre for Experimental and Clinical Infection Research, a Joint Venture Between the Hannover Medical School and the Helmholtz Centre for Infection Research, Hannover, Germany.

Frontiers in Immunology
|March 31, 2022
PubMed
Summary

Staphylococcus aureus uses adenosine synthase A (AdsA) to produce deoxyadenosine and deoxyguanosine. These molecules kill immune cells, helping the dangerous bacteria survive and cause severe infections.

Keywords:
Staphylococcus aureusapoptosisdeoxyguanosinedeoxyribonucleosidesimmune evasionmacrophagephagocyte

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Studying Interactions of Staphylococcus aureus with Neutrophils by Flow Cytometry and Time Lapse Microscopy
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Development and Assessment of Intracellular Infection Models for Staphylococcus aureus
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Development and Assessment of Intracellular Infection Models for Staphylococcus aureus
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Development and Assessment of Intracellular Infection Models for Staphylococcus aureus

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Area of Science:

  • Microbiology
  • Immunology
  • Biochemistry

Background:

  • Staphylococcus aureus is a major human pathogen causing life-threatening infections.
  • Adenosine synthase A (AdsA) is a known virulence factor involved in staphylococcal pathogenesis.
  • AdsA contributes to bacterial survival by targeting host immune cells.

Purpose of the Study:

  • To investigate the full enzymatic activity of AdsA beyond deoxyadenosine production.
  • To identify the mechanisms by which S. aureus evades host immune responses.
  • To explore novel therapeutic targets against multidrug-resistant S. aureus.

Main Methods:

  • Multi-technological approach including in vitro assays.
  • Genome-wide CRISPR-Cas9 knock-out screening.
  • Analysis of host-pathogen interactions in abscess-mimicking environments.

Main Results:

  • AdsA excessively synthesizes cytotoxic deoxyguanosine (dGuo) in addition to deoxyadenosine (dAdo).
  • dGuo and dAdo target the purine salvage pathway-apoptosis axis in phagocytes.
  • S. aureus utilizes multiple deoxyribonucleosides to induce host cell death and enhance survival.

Conclusions:

  • S. aureus employs a sophisticated strategy using multiple cytotoxic deoxyribonucleosides to overcome host defenses.
  • AdsA plays a dual role in generating both dAdo and dGuo, crucial for bacterial virulence.
  • Understanding these mechanisms offers potential for developing new treatments against S. aureus infections.