Related Experiment Videos

Protein kinase C activation and vacuolation in HeLa cells invaded by Mycoplasma penetrans

Z Borovsky1, M Tarshis, P Zhang

  • 1Department of Membrane and Ultrastructure Research, The Hebrew University-Hadassah Medical School, Jerusalem, Israel.

Insights

Mycoplasma penetrans, an AIDS-associated bacterium, invades non-phagocytic HeLa cells by hijacking host cell machinery. This invasion involves cytoskeletal rearrangement and leads to cellular damage, including vacuolation and increased peroxide levels.

Area of Science:

  • Cell biology
  • Microbiology
  • Immunology

Background:

  • Mycoplasma penetrans is an opportunistic pathogen associated with Acquired Immunodeficiency Syndrome (AIDS).
  • Non-phagocytic cells, such as HeLa cells, are typically resistant to bacterial invasion.
  • Understanding pathogen-host interactions is crucial for developing therapeutic strategies.

Purpose of the Study:

  • To investigate the mechanism of Mycoplasma penetrans invasion into HeLa cells.
  • To elucidate the cellular consequences of this invasion.
  • To identify potential host factors involved in M. penetrans entry.

Main Methods:

  • Confocal laser scanning microscopy was used to visualize and quantify bacterial invasion.
  • Inhibition of cytoskeletal components (microfilaments and microtubules) using cytochalasin D, vinblastine, and taxol.
  • Biochemical assays to detect protein kinase C activation and intracellular organic peroxide levels.
  • Alpha-tocopherol was used to mitigate peroxide accumulation.

Main Results:

  • M. penetrans invasion of HeLa cells is dependent on infection duration and temperature.
  • Invasion requires intact microfilaments and microtubules, indicating cytoskeletal involvement.
  • Short-term infection activates protein kinase C; prolonged infection causes vacuolation and increased intracellular peroxides.
  • Preventing peroxide accumulation partially reduced vacuolation.

Conclusions:

  • Mycoplasma penetrans actively invades non-phagocytic HeLa cells.
  • Bacterial entry is mediated by host cell cytoskeleton dynamics and signaling pathways.
  • Cellular damage, including vacuolation and oxidative stress, results from prolonged M. penetrans infection.

Related Concept Videos