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Serratia marcescens is able to survive and proliferate in autophagic-like vacuoles inside non-phagocytic cells

Griselda V Fedrigo1, Emanuel M Campoy, Gisela Di Venanzio

  • 1Instituto de Biología Molecular y Celular de Rosario (IBR-CONICET), Departamento de Microbiología, Facultad de Ciencias Bioquímicas y Farmacéuticas, Universidad Nacional de Rosario, Rosario, Argentina.

Plos One
|September 9, 2011
PubMed

Insights

Serratia marcescens, a problematic opportunistic pathogen, invades host cells and creates a protected niche by manipulating cellular autophagy. This allows the bacteria to survive and multiply within a non-acidic compartment, evading degradation.

Area of Science:

  • Microbiology
  • Cell Biology
  • Pathogenesis

Background:

  • Serratia marcescens is an opportunistic pathogen causing significant public health concerns, especially in vulnerable populations.
  • Mechanisms underlying S. marcescens pathogenesis remain poorly understood.

Purpose of the Study:

  • To investigate the invasion process and intracellular survival mechanisms of Serratia marcescens in host epithelial cells.
  • To elucidate how S. marcescens interacts with cellular pathways like autophagy.

Main Methods:

  • Cell culture experiments using epithelial cells.
  • Microscopy techniques to visualize bacterial localization and cellular compartment markers (LC3, Rab7).
  • Analysis of vacuole properties (acidity, degradative capacity).

Main Results:

  • Serratia marcescens invades epithelial cells and persists within a large, membrane-bound compartment.
  • This compartment exhibits autophagic-like features, recruiting LC3 and Rab7.
  • The majority of these compartments are non-acidic and non-degradative, suggesting evasion of lysosomal fusion.
  • S. marcescens also triggers a non-canonical autophagic process prior to internalization.

Conclusions:

  • Serratia marcescens actively manipulates host cell autophagic pathways for intracellular survival.
  • The bacteria establish a protected niche by altering autophagosome maturation and preventing lysosomal degradation.
  • These findings reveal novel strategies employed by S. marcescens to proliferate within host cells.

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