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The Extrinsic Apoptotic Pathway01:17

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The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
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Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
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The Intrinsic Apoptotic Pathway01:31

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Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
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Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size...
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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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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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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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Intracellular Staphylococcus aureus and host cell death pathways.

Ye Mon Soe1, Sammy Bedoui1, Timothy P Stinear1

  • 1Department of Microbiology and Immunology, University of Melbourne at the Peter Doherty Institute for Infection and Immunity, Melbourne, Victoria, Australia.

Cellular Microbiology
|February 7, 2021
PubMed
Summary
This summary is machine-generated.

Staphylococcus aureus evades host programmed cell death (PCD) by modulating virulence factors during its intracellular lifestyle. Understanding this interplay is key to combating S. aureus infections.

Keywords:
PCDStaphylococcus aureusapoptosisautophagyferroptosisintracellular pathogenmetabolismnecroptosisprogrammed cell deathpyroptosis

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Area of Science:

  • Microbiology
  • Immunology
  • Pathogenesis

Background:

  • Staphylococcus aureus is a prevalent opportunistic human pathogen.
  • Intracellular lifestyle aids S. aureus in evading host immunity and antibiotics.
  • Host programmed cell death (PCD) pathways pose a threat to intracellular bacteria.

Purpose of the Study:

  • To review the interplay between S. aureus virulence factors and host PCD pathways.
  • To analyze how S. aureus adapts to evade elimination by PCD.
  • To identify future research directions in S. aureus-PCD interactions.

Main Methods:

  • Literature review of current research on S. aureus pathogenesis.
  • Analysis of S. aureus virulence factors and their role in immune evasion.
  • Examination of host PCD mechanisms including apoptosis, pyroptosis, and necroptosis.

Main Results:

  • S. aureus utilizes pathoadaptive mechanisms to modulate virulence factor expression.
  • Bacterial adaptation to the intracellular environment is crucial for evading PCD.
  • Interplay between bacterial virulence and host cell death pathways is complex.

Conclusions:

  • S. aureus actively manipulates host PCD pathways for survival.
  • Understanding bacterial evasion strategies is critical for developing new therapeutics.
  • Further research is needed to fully elucidate S. aureus-PCD interactions.