A process for controlling intracellular bacterial infections induced by membrane injury

Deepannita Roy1, David R Liston, Vincent J Idone

  • 1Section of Microbial Pathogenesis and Department of Cell Biology, Yale University School of Medicine, New Haven, CT 06510, USA.

Science (New York, N.Y.)
|June 5, 2004
PubMed

Insights

Lysosomal synaptotagmin Syt VII promotes phagolysosome fusion, limiting bacterial growth. This calcium-dependent mechanism, akin to lysosomal repair, protects cells from pathogens that disrupt membranes.

Area of Science:

  • Cell Biology
  • Immunology
  • Microbiology

Background:

  • Phagolysosome fusion is critical for pathogen clearance.
  • Inhibiting this fusion aids intracellular pathogen survival.

Purpose of the Study:

  • Investigate the role of lysosomal synaptotagmin Syt VII in phagolysosome fusion.
  • Determine if Syt VII mediates a cellular defense mechanism against bacterial pathogens.

Main Methods:

  • Utilized Syt VII knockout (Syt VII -/-) and wild-type (Syt VII +/+) cells.
  • Examined calcium-dependent phagolysosome fusion.
  • Assessed intracellular bacterial survival following type III secretion system (T3SS) activation.

Main Results:

  • Syt VII is essential for calcium-dependent phagolysosome fusion.
  • This fusion mechanism limits intracellular growth of pathogenic bacteria.
  • Bacterial T3SS-induced membrane permeabilization and calcium influx trigger lysosomal exocytosis, inhibiting bacterial survival in Syt VII +/+ but not Syt VII -/- cells.

Conclusions:

  • Lysosomal Syt VII mediates a repair-like mechanism promoting phagolysosome fusion.
  • This pathway restricts intracellular bacterial proliferation.
  • Cellular responses to membrane injury can confer resistance to certain bacterial pathogens.

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