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Pneumococcus Infection of Primary Human Endothelial Cells in Constant Flow

Published on: October 31, 2019

Chlamydia pneumoniae facilitates monocyte adhesion to endothelial and smooth muscle cells

R Kaul1, W M Wenman

  • 1Section of Infectious Diseases, Department of Pediatrics, University of California Davis, CA 95616, USA. rkkaul@ucdavis.edu

Microbial Pathogenesis
|March 29, 2001
PubMed

Insights

Chlamydia pneumoniae can infect human monocytes, enabling them to adhere to artery cells. This suggests a mechanism for how Chlamydia pneumoniae contributes to atherosclerosis development.

Area of Science:

  • Infectious diseases
  • Cardiovascular research
  • Cell biology

Background:

  • Chlamydia pneumoniae infection is associated with atherosclerotic heart disease.
  • The mechanism by which C. pneumoniae accesses atheromatous lesions remains unclear.
  • Infected circulatory components adhering to vascular cells may initiate inflammation.

Purpose of the Study:

  • To investigate the susceptibility of human monocytes to C. pneumoniae infection.
  • To determine if C. pneumoniae-infected monocytes adhere to human coronary artery endothelial cells (HCAEC) and smooth muscle cells (HCSMC).

Main Methods:

  • Human monocytes were infected in vitro with viable or heat-inactivated C. pneumoniae.
  • Infection was confirmed by observing chlamydial inclusions.
  • Adherence of infected and uninfected monocytes to HCAEC and HCSMC was quantified.

Main Results:

  • Monocytes were successfully infected by viable C. pneumoniae, showing characteristic inclusions.
  • Heat-inactivated C. pneumoniae did not infect monocytes, with no inclusions observed.
  • Monocytes infected with viable C. pneumoniae exhibited significantly increased adherence to HCAEC and HCSMC.

Conclusions:

  • Human monocytes are susceptible to C. pneumoniae infection in vitro.
  • C. pneumoniae infection enhances monocyte adherence to coronary artery cells.
  • This enhanced adherence may represent a key step in C. pneumoniae's role in atherosclerosis pathogenesis.

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