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Chlamydia pneumoniae entry into epithelial cells by clathrin-independent endocytosis

Juha T Korhonen1, Mirja Puolakkainen, Anu Haveri

  • 1Turku Centre for Biotechnology, University of Turku and Åbo Akademi University, Turku, Finland. juha.korhonen@utu.fi

Microbial Pathogenesis
|December 29, 2011
PubMed

Insights

Chlamydia pneumoniae invasion into lung cells depends on cholesterol and sphingomyelin in cell membranes, not clathrin. Scavenger receptor B, type I (SR-BI) supports bacterial growth within cells.

Area of Science:

  • Microbiology
  • Cell Biology
  • Pathogen-Host Interactions

Background:

  • Chlamydia pneumoniae is a common respiratory pathogen.
  • Understanding its invasion mechanisms is crucial for developing treatments.

Purpose of the Study:

  • To investigate the role of host cell plasma membrane composition in Chlamydia pneumoniae invasion.
  • To determine the involvement of clathrin and scavenger receptor B, type I (SR-BI) in C. pneumoniae entry.

Main Methods:

  • Manipulating host cell cholesterol levels using methyl-beta-cyclodextrin (MβCD) and cholesterol-complexed MβCD.
  • Using cholesterol-sequestering agents (nystatin, filipin) and sphingomyelinase.
  • Employing RNA interference to silence clathrin and SR-BI in A549 lung epithelial cells.

Main Results:

  • Cholesterol depletion inhibited C. pneumoniae invasion, while cholesterol loading enhanced it.
  • Invasion was reduced by nystatin, filipin, and sphingomyelinase.
  • C. pneumoniae entry was independent of clathrin and SR-BI, but SR-BI silencing attenuated bacterial growth.

Conclusions:

  • C. pneumoniae attachment and invasion rely on cholesterol- and sphingomyelin-rich membrane microdomains.
  • The entry process is clathrin-independent.
  • SR-BI plays a role in supporting C. pneumoniae growth within epithelial cells.

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