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Invasion of human epithelial cells by Pseudomonas aeruginosa involves src-like tyrosine kinases p60Src and p59Fyn

M Esen1, H Grassmé, J Riethmüller

  • 1Department of Physiology, University of Tuebingen, 72076 Tuebingen, Germany.

Infection and Immunity
|December 19, 2000
PubMed

Insights

Pseudomonas aeruginosa invasion into human cells requires Src-like tyrosine kinases (Src and Fyn). Inhibiting these kinases blocks bacterial entry but not adhesion, revealing a key mechanism in infection.

Area of Science:

  • Microbiology
  • Cell Biology
  • Biochemistry

Background:

  • Pseudomonas aeruginosa is a significant pathogen in cystic fibrosis and immunocompromised patients.
  • Bacterial internalization by host cells is crucial for infection but poorly understood.
  • P. aeruginosa is known to be internalized by human epithelial cells.

Purpose of the Study:

  • To elucidate the molecular mechanisms of P. aeruginosa internalization into human epithelial cells.
  • To investigate the role of Src-like tyrosine kinases in bacterial invasion.

Main Methods:

  • Studied P. aeruginosa internalization in human epithelial cells.
  • Investigated the activation of Src-like tyrosine kinases (p59Fyn and p60Src).
  • Utilized kinase inhibitors to assess the impact on bacterial internalization and adhesion.

Main Results:

  • P. aeruginosa internalization triggers Src and Fyn activation and protein tyrosine phosphorylation.
  • Inhibition of Src-like tyrosine kinases significantly blocked bacterial internalization, but not adhesion.
  • Blocking P. aeruginosa binding to CFTR also prevented Src and Fyn activation.

Conclusions:

  • Src-like tyrosine kinases (Src and Fyn) are essential for P. aeruginosa invasion into human epithelial cells.
  • These kinases play a pivotal role in the internalization process, distinct from bacterial adhesion.
  • Targeting Src-like tyrosine kinases may offer a strategy to combat P. aeruginosa infections.

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